PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8862010-3 1996 In cisplatin-sensitive HL-60 cells, which express the MRP/GS-X pump at low levels, c-myc expression was substantially suppressed by delta(7)-PGA1 methyl ester and the cell cycle was arrested in G1 phase. Cisplatin 3-12 MYC proto-oncogene, bHLH transcription factor Homo sapiens 83-88 8760592-2 1996 However, transfection of c-myc or v-H-ras and activation of protein kinase C (PKC), which contributes to the RAF-1, MAP kinase signal transduction pathway, can influence therapeutic response to CDDP. Cisplatin 194-198 MYC proto-oncogene, bHLH transcription factor Homo sapiens 25-30 8712728-11 1996 These findings suggest that c-myc plays a role in cDDP resistance by effects other than those on cell cycle distribution. Cisplatin 50-54 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 7694127-3 1993 The aim of this study was to examine whether the development of resistance to cisplatin and vincristine changes the expression of c-myc and c-Ki-ras oncogenes and to determine whether there is a correlation between the expression of these oncogenes and the sensitivity of selected clones to cisplatin, methotrexate and gamma-rays. Cisplatin 78-87 MYC proto-oncogene, bHLH transcription factor Homo sapiens 130-135 7827130-10 1995 Treatment with VP-16 or CDDP significantly induced c-myc mRNA levels in sensitive PC3 cells. Cisplatin 24-28 MYC proto-oncogene, bHLH transcription factor Homo sapiens 51-56 7923012-0 1994 Enhancement of sensitivity of urinary bladder tumor cells to cisplatin by c-myc antisense oligonucleotide. Cisplatin 61-70 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-79 7923012-10 1994 However, combination treatment with the c-myc antisense oligonucleotide and CDDP resulted in a synergistic cytotoxic effect on T24 cells and two freshly derived UBT cells. Cisplatin 76-80 MYC proto-oncogene, bHLH transcription factor Homo sapiens 40-45 7923012-11 1994 Further, treatment of CDDP-resistant T24 cells (T24/CDDP) with c-myc antisense oligonucleotide and CDDP reversed the resistance. Cisplatin 22-26 MYC proto-oncogene, bHLH transcription factor Homo sapiens 63-68 7923012-11 1994 Further, treatment of CDDP-resistant T24 cells (T24/CDDP) with c-myc antisense oligonucleotide and CDDP reversed the resistance. Cisplatin 52-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 63-68 7923012-11 1994 Further, treatment of CDDP-resistant T24 cells (T24/CDDP) with c-myc antisense oligonucleotide and CDDP reversed the resistance. Cisplatin 52-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 63-68 7923012-14 1994 Incubation of T24 or T24/CDDP cells with the c-myc antisense oligonucleotide increased the intracellular accumulation of CDDP, but not the accumulation of 5-FU. Cisplatin 25-29 MYC proto-oncogene, bHLH transcription factor Homo sapiens 45-50 7923012-14 1994 Incubation of T24 or T24/CDDP cells with the c-myc antisense oligonucleotide increased the intracellular accumulation of CDDP, but not the accumulation of 5-FU. Cisplatin 121-125 MYC proto-oncogene, bHLH transcription factor Homo sapiens 45-50 7923012-15 1994 CONCLUSIONS: This study demonstrates that combination treatment with c-myc antisense oligonucleotide and CDDP can overcome the CDDP-resistance of UBT cells and that the increased intracellular accumulation of CDDP by c-myc antisense oligonucleotide may play a role in the enhanced cytotoxicity obtained. Cisplatin 105-109 MYC proto-oncogene, bHLH transcription factor Homo sapiens 217-222 7923012-15 1994 CONCLUSIONS: This study demonstrates that combination treatment with c-myc antisense oligonucleotide and CDDP can overcome the CDDP-resistance of UBT cells and that the increased intracellular accumulation of CDDP by c-myc antisense oligonucleotide may play a role in the enhanced cytotoxicity obtained. Cisplatin 127-131 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-74 7923012-15 1994 CONCLUSIONS: This study demonstrates that combination treatment with c-myc antisense oligonucleotide and CDDP can overcome the CDDP-resistance of UBT cells and that the increased intracellular accumulation of CDDP by c-myc antisense oligonucleotide may play a role in the enhanced cytotoxicity obtained. Cisplatin 127-131 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-74 7923012-16 1994 The synergistic effect obtained with established UBT cells and freshly isolated UBT cells suggests that combination treatment with c-myc antisense oligonucleotide and CDDP may have clinical application in the therapy of CDDP-resistant UBT. Cisplatin 220-224 MYC proto-oncogene, bHLH transcription factor Homo sapiens 131-136 2009531-0 1991 Modulation of cis-platinum resistance in Friend erythroleukemia cells by c-myc. Cisplatin 14-26 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-78 1806037-0 1991 The effect of cisplatin and carboplatin on c-myc promoter in erythroleukemic cells. Cisplatin 14-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 43-48 1806037-4 1991 These results demonstrate that cisplatin stimulates transcription from the c-myc promoter in erythroleukemia cells and may support the use of carboplatin as compared to cisplatin in the treatment of cancer patients. Cisplatin 31-40 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-80 1806037-4 1991 These results demonstrate that cisplatin stimulates transcription from the c-myc promoter in erythroleukemia cells and may support the use of carboplatin as compared to cisplatin in the treatment of cancer patients. Cisplatin 169-178 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-80 1888169-3 1991 At 5 X 10(-5) M concentration cis-platin stimulates cat gene expression 9 and 11 fold respectively in cell lines containing constructs with c-myc promoter sequences truncated at -2319 and -350 relative to c-myc RNA start site P1. Cisplatin 30-40 MYC proto-oncogene, bHLH transcription factor Homo sapiens 140-145 1888169-3 1991 At 5 X 10(-5) M concentration cis-platin stimulates cat gene expression 9 and 11 fold respectively in cell lines containing constructs with c-myc promoter sequences truncated at -2319 and -350 relative to c-myc RNA start site P1. Cisplatin 30-40 MYC proto-oncogene, bHLH transcription factor Homo sapiens 205-210 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-4 1991 We tested this hypothesis by determining the effect of varying the level of c-myc expression on resistance to cis-platinum and ionizing radiation in Friend murine erythroleukemia cells expressing varying levels of c-myc gene product. Cisplatin 110-122 MYC proto-oncogene, bHLH transcription factor Homo sapiens 78-81 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 31-43 MYC proto-oncogene, bHLH transcription factor Homo sapiens 95-98 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 31-43 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 31-43 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 31-43 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 31-43 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2009531-5 1991 We found that a) the degree of cis-platinum resistance correlated directly with the level of c-myc expression, b) glucocorticoid induction of murine mammary tumor virus promoter-driven c-myc sequences significantly increased cis-platinum resistance, c) restoring c-myc transcript levels to normal restored the original cis-platinum sensitivity at a rate which paralleled that of induced c-myc transcript depletion, and d) c-myc transcript level had no effect on ionizing radiation response. Cisplatin 225-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-190 2064352-0 1991 Coordinate change of c-myc, transferrin receptor and H3 gene expression precedes induction of haemoglobin-producing cells of the leukaemia K562 cell line treated with cis-diamminedichloroplatinum (II). Cisplatin 167-195 MYC proto-oncogene, bHLH transcription factor Homo sapiens 21-26 2064352-8 1991 Five days after CDDP treatment, the expression of c-myc oncogene had risen, while H3 histone mRNA expression fell to undetectable levels within 24 hours. Cisplatin 16-20 MYC proto-oncogene, bHLH transcription factor Homo sapiens 50-55 34948122-8 2021 Simultaneously, endogenous MYC was remarkably activated by PARP1, thereby repressing the BIN1 promoter, whereas PARP inhibition abolished the hyperactivated MYC-dependent BIN1 suppression and restored cisplatin sensitivity. Cisplatin 201-210 MYC proto-oncogene, bHLH transcription factor Homo sapiens 27-30 2113532-10 1990 Thus, cisplatin treatment in A2780DDP cells differentially induces expression of certain nuclear oncogenes (c-fos/c-myc), as well as genes possibly involved in the repair of cisplatin-mediated DNA damage, an induction suppressed by CSA treatment. Cisplatin 6-15 MYC proto-oncogene, bHLH transcription factor Homo sapiens 114-119 34948122-3 2021 Here, we report that the coordinated actions of MYC, PARP1, and ATM assist cancer cells in acquiring cisplatin resistance by BIN1 deficits. Cisplatin 101-110 MYC proto-oncogene, bHLH transcription factor Homo sapiens 48-51 34769137-7 2021 Mitigated cisplatin chemoresistance was associated with the concurrent suppression of c-Myc expression in T24/R cells. Cisplatin 10-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 86-91 32725721-10 2020 We also found that enhanced MYC signaling, ribosomal biogenesis, glycolysis, and mitochondrial respiration are key signatures in OS cells with cisplatin resistance. Cisplatin 143-152 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-31 34204834-6 2021 Decreased c-MYC expression in PE/CA-PJ49 treated with CisPt + RSV was accompanied by cell cycle blockage in G0/G1 phase. Cisplatin 54-59 MYC proto-oncogene, bHLH transcription factor Homo sapiens 10-15 35626088-11 2022 Notably, intrinsic resistance was conquered by Cisplatin because of cMYC and IDO-1 downregulation. Cisplatin 47-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 68-72 32626933-6 2020 The present study demonstrated that FBP1 and its target, c-Myc, were more highly expressed in breast cancer tissues compared with para-carcinoma tissues, and the FBP1 and c-Myc levels are decreased by cisplatin treatment. Cisplatin 201-210 MYC proto-oncogene, bHLH transcription factor Homo sapiens 57-62 32626933-6 2020 The present study demonstrated that FBP1 and its target, c-Myc, were more highly expressed in breast cancer tissues compared with para-carcinoma tissues, and the FBP1 and c-Myc levels are decreased by cisplatin treatment. Cisplatin 201-210 MYC proto-oncogene, bHLH transcription factor Homo sapiens 171-176 34232919-9 2021 Mechanistically, MBZ was revealed to inhibit multiple cancer-related signal pathways including ELK/SRF, NFKB, MYC/MAX, and E2F/DP1 in cisplatin-resistant ovarian cancer cells. Cisplatin 134-143 MYC proto-oncogene, bHLH transcription factor Homo sapiens 110-113 34204834-4 2021 In FaDu cells, combined CisPt + RSV treatment induced an increase in apoptosis, which was associated with an increase in c-MYC and TP53 and a decrease in BCL-2 expression. Cisplatin 24-29 MYC proto-oncogene, bHLH transcription factor Homo sapiens 121-126 35070983-14 2021 Furthermore, quercetin combined with cisplatin downregulated the expression of EGFR, MYC, CCND1, and ERBB2 proteins and upregulated CASP8 expression in HeLa and SiHa cells. Cisplatin 37-46 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-88 35173547-9 2022 Additionally, we investigated that silencing HJURP increased sensitivity of ovarian cancer cells to cisplatin via MYC/WEE1 axis, and HJURP participated in DNA repair of cisplatin-induced damage. Cisplatin 100-109 MYC proto-oncogene, bHLH transcription factor Homo sapiens 114-117 32710593-8 2020 CONCLUSION: Nanog directly participated in the regulation of Slug, E-cadherin, Oct-4, and c-Myc genes, causing cisplatin resistance/recurrence of OSCC. Cisplatin 111-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 90-95 31821542-7 2020 In summary, our findings suggest that the miR-145/c-Myc/PD-L1 axis contributes to cisplatin resistance in ovarian cancer and support that miR-145 might act as an adjuvant therapeutic target in chemotherapy of ovarian cancer. Cisplatin 82-91 MYC proto-oncogene, bHLH transcription factor Homo sapiens 50-55 33488948-3 2020 TNBC cells treated with CFM-4.16 plus cisplatin inhibited the expression of FZD8, LRP6 and c-Myc and significantly enhanced cell death in all the cell lines by ~70%-80% compared with the control(s). Cisplatin 38-47 MYC proto-oncogene, bHLH transcription factor Homo sapiens 91-96 32319562-4 2020 Furthermore, the TAM-resistant cells were significantly more sensitive to cisplatin compared with the parent cells, and the silencing of c-MYC expression desensitized the cells to cisplatin through the inhibition of the cell cycle. Cisplatin 180-189 MYC proto-oncogene, bHLH transcription factor Homo sapiens 137-142 32319562-5 2020 An increased c-MYC expression was observed in 28 pairs of primary and metastatic tumors from patients treated with TAM, and the clinical remission rate of cisplatin-based chemotherapy was significantly higher compared with other chemotherapy-based regimens in 122 patients with TAM resistant breast cancer. Cisplatin 155-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 13-18 32319562-6 2020 Taken together, the data of the present study demonstrated that although c-MYC was involved in TAM resistance, it increased the sensitivity of ER+ breast cancer to cisplatin. Cisplatin 164-173 MYC proto-oncogene, bHLH transcription factor Homo sapiens 73-78 33089188-10 2020 Combination treatment of DEC1 overexpression and cisplatin inhibited apoptosis and affected SOX2 and c-MYC expressions in HeLa cells. Cisplatin 49-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 101-106 31765939-11 2020 The combination of cisplatin and hypoxia led to sustained c-Myc protein expression in wildtype cells. Cisplatin 19-28 MYC proto-oncogene, bHLH transcription factor Homo sapiens 58-63 31632022-11 2019 Cisplatin-induced c-Myc was found to directly bind the miR-425-3p promoter and transactivated its expression. Cisplatin 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 31761897-0 2019 Forkhead Box R2 Knockdown Decreases Chemoresistance to Cisplatin via MYC Pathway in Bladder Cancer. Cisplatin 55-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-72 31761897-12 2019 CONCLUSIONS FoxR2 knockdown decreases chemoresistance to cisplatin via the MYC pathway in bladder cancer cells, and this may be a target for overcoming chemoresistance in bladder cancer. Cisplatin 57-66 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-78 31727874-0 2019 Cisplatin exposure causes c-Myc-dependent resistance to CDK4/6 inhibition in HPV-negative head and neck squamous cell carcinoma. Cisplatin 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 26-31 31727874-6 2019 Mechanistically, in the course of provoking a DNA damage-resistance phenotype, cisplatin exposure upregulates both c-Myc and cyclin E, and combination treatment with palbociclib and the c-Myc bromodomain inhibitor JQ1 exerts a synergistic anti-growth effect in cisplatin-resistant cells. Cisplatin 79-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 115-120 31727874-6 2019 Mechanistically, in the course of provoking a DNA damage-resistance phenotype, cisplatin exposure upregulates both c-Myc and cyclin E, and combination treatment with palbociclib and the c-Myc bromodomain inhibitor JQ1 exerts a synergistic anti-growth effect in cisplatin-resistant cells. Cisplatin 79-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 186-191 31727874-6 2019 Mechanistically, in the course of provoking a DNA damage-resistance phenotype, cisplatin exposure upregulates both c-Myc and cyclin E, and combination treatment with palbociclib and the c-Myc bromodomain inhibitor JQ1 exerts a synergistic anti-growth effect in cisplatin-resistant cells. Cisplatin 261-270 MYC proto-oncogene, bHLH transcription factor Homo sapiens 186-191 31727874-7 2019 These data show the benefit of exploiting the inherent resistance mechanisms of HNSCC to overcome cisplatin- and palbociclib resistance through the use of c-Myc inhibition. Cisplatin 98-107 MYC proto-oncogene, bHLH transcription factor Homo sapiens 155-160 31432162-6 2019 Cisplatin also induced Bcl-2-associated X protein expression, and decreased that of Bcl-2 and c-Myc in lung adenocarcinoma cells. Cisplatin 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 94-99 30825244-8 2019 c-Myc- and SNHG12 overexpression promoted proliferation and inhibited sensitivity to cisplatin (CDDP) in NK/T-cell lymphoma cell line YTS cells, and c-Myc and SNHG12-downregulation inhibited proliferation and enhanced sensitivity to CDDP in SNK-6 cells. Cisplatin 85-94 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 30825244-8 2019 c-Myc- and SNHG12 overexpression promoted proliferation and inhibited sensitivity to cisplatin (CDDP) in NK/T-cell lymphoma cell line YTS cells, and c-Myc and SNHG12-downregulation inhibited proliferation and enhanced sensitivity to CDDP in SNK-6 cells. Cisplatin 96-100 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 30825244-8 2019 c-Myc- and SNHG12 overexpression promoted proliferation and inhibited sensitivity to cisplatin (CDDP) in NK/T-cell lymphoma cell line YTS cells, and c-Myc and SNHG12-downregulation inhibited proliferation and enhanced sensitivity to CDDP in SNK-6 cells. Cisplatin 233-237 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 30825244-12 2019 Further research showed that SNHG12 overexpression reversed the effects of c-Myc downregulation on proliferation and sensitivity to CDDP in NKTCL cell lines. Cisplatin 132-136 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-80 30210134-0 2019 Gemcitabine, Dexamethasone, and Cisplatin Regimen as an Effective Salvage Therapy for High-grade B-cell Lymphoma with MYC and BCL2 and/or BCL6 Rearrangements. Cisplatin 32-41 MYC proto-oncogene, bHLH transcription factor Homo sapiens 118-121 30668336-0 2019 Ailanthone inhibits cell growth and migration of cisplatin resistant bladder cancer cells through down-regulation of Nrf2, YAP, and c-Myc expression. Cisplatin 49-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 132-137 30668336-21 2019 Its high effectiveness in CDDP resistant cells could be related to the inhibition of Nrf2, YAP, and c-Myc expressions. Cisplatin 26-30 MYC proto-oncogene, bHLH transcription factor Homo sapiens 100-105 31186712-8 2019 In summary, the current study demonstrated that inhibition of BMI1 and Mel18 could increase the sensitivity of esophageal cancer cells to cisplatin via inhibition of c-Myc. Cisplatin 138-147 MYC proto-oncogene, bHLH transcription factor Homo sapiens 166-171 30166592-0 2019 miR-137 mediates the functional link between c-Myc and EZH2 that regulates cisplatin resistance in ovarian cancer. Cisplatin 75-84 MYC proto-oncogene, bHLH transcription factor Homo sapiens 45-50 31933859-5 2019 Finally, c-MYC, OCT4 and p53 were determined to contribute to the transcriptional regulation of NEAT1.1 under cisplatin using ChIP assay. Cisplatin 110-119 MYC proto-oncogene, bHLH transcription factor Homo sapiens 9-14 30166592-9 2019 Thus, our studies elucidate a novel role of miR-137 in regulating c-Myc-EZH2 axis that is crucial to the regulation of cisplatin resistance in ovarian cancer. Cisplatin 119-128 MYC proto-oncogene, bHLH transcription factor Homo sapiens 66-71 30166592-2 2019 Although both c-Myc and EZH2 have been implicated in regulating cisplatin resistance in ovarian cancer, the interplay between these two regulators is poorly understood. Cisplatin 64-73 MYC proto-oncogene, bHLH transcription factor Homo sapiens 14-19 30166592-3 2019 Using RNA sequence analysis (RNA-seq), for the first time we find that miR-137 level is extremely low in cisplatin resistant ovarian cancer cells, correlating with higher levels of c-Myc and EZH2 expression. Cisplatin 105-114 MYC proto-oncogene, bHLH transcription factor Homo sapiens 181-186 30166592-4 2019 Further analyses indicate that in resistant cells c-Myc enhances the expression of EZH2 by directly suppressing miR-137 that targets EZH2 mRNA, and increased expression of EZH2 activates cellular survival pathways, resulting in the resistance to cisplatin. Cisplatin 246-255 MYC proto-oncogene, bHLH transcription factor Homo sapiens 50-55 30166592-5 2019 Inhibition of c-Myc-miR-137-EZH2 pathway re-sensitizes resistant cells to cisplatin. Cisplatin 74-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 14-19 30166592-6 2019 Both in vivo and in vitro analyses indicate that cisplatin treatment activates c-Myc-miR-137-EZH2 pathway. Cisplatin 49-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 79-84 30071534-13 2018 RESULTS: In cisplatin-resistant A2780CDDP cells, HDAC1 knockdown by siRNA suppressed cell proliferation, and increased apoptosis and chemosensitivity by downregulating c-Myc and upregulating miR-34a. Cisplatin 12-21 MYC proto-oncogene, bHLH transcription factor Homo sapiens 168-173 30443189-10 2018 Further investigation showed that RIF1 regulated the expression of MYC and MYC downstream targets, including the cell cycle and double-stranded break (DSB) repair genes which might mediate the effect of RIF1 on cellular response to cisplatin. Cisplatin 232-241 MYC proto-oncogene, bHLH transcription factor Homo sapiens 67-70 30443189-10 2018 Further investigation showed that RIF1 regulated the expression of MYC and MYC downstream targets, including the cell cycle and double-stranded break (DSB) repair genes which might mediate the effect of RIF1 on cellular response to cisplatin. Cisplatin 232-241 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-78 30443189-12 2018 Taken together, these data revealed that RIF1 played an important role in regulating MYC and MYC-activated genes, which in turn contributes to cellular response to cisplatin and NSCLC patients" response to platinum-based chemotherapy. Cisplatin 164-173 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-88 30443189-12 2018 Taken together, these data revealed that RIF1 played an important role in regulating MYC and MYC-activated genes, which in turn contributes to cellular response to cisplatin and NSCLC patients" response to platinum-based chemotherapy. Cisplatin 164-173 MYC proto-oncogene, bHLH transcription factor Homo sapiens 93-96 29257330-0 2018 Niclosamide enhances the cytotoxic effect of cisplatin in cisplatin-resistant human lung cancer cells via suppression of lung resistance-related protein and c-myc. Cisplatin 45-54 MYC proto-oncogene, bHLH transcription factor Homo sapiens 157-162 29257330-7 2018 The expression levels of cisplatin-resistant-associated molecules (lung resistance-related protein and c-myc) following niclosamide treatment in A549/DDP cells were evaluated by western blot analysis. Cisplatin 25-34 MYC proto-oncogene, bHLH transcription factor Homo sapiens 103-108 29286162-6 2018 Further research revealed that the upregulation of p-STAT3 and c-Myc which was induced by the single treatment with either cisplatin or GC7 was significantly reversed by the GC7/cisplatin combination in mesenchymal phenotype Tca8113 and HN30 cells. Cisplatin 123-132 MYC proto-oncogene, bHLH transcription factor Homo sapiens 63-68 29286162-6 2018 Further research revealed that the upregulation of p-STAT3 and c-Myc which was induced by the single treatment with either cisplatin or GC7 was significantly reversed by the GC7/cisplatin combination in mesenchymal phenotype Tca8113 and HN30 cells. Cisplatin 178-187 MYC proto-oncogene, bHLH transcription factor Homo sapiens 63-68 30071534-17 2018 c-Myc re-expression or miR-34a targeting by miR-34a inhibitors protected cells from apoptosis or reversed cisplatin resistance following HDAC1 knockdown or/and cisplatin exposure. Cisplatin 106-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 30071534-17 2018 c-Myc re-expression or miR-34a targeting by miR-34a inhibitors protected cells from apoptosis or reversed cisplatin resistance following HDAC1 knockdown or/and cisplatin exposure. Cisplatin 160-169 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 30071534-21 2018 Thus, targeting HDAC1 by enhancing c-Myc-dependent miR-34a expression might be an effective strategy for increasing the efficacy of cisplatin treatment. Cisplatin 132-141 MYC proto-oncogene, bHLH transcription factor Homo sapiens 35-40 30071534-15 2018 Cisplatin treatment activated HDAC1 and c-Myc and inactivated miR-34a. Cisplatin 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 40-45 29060932-0 2017 miR-34a increases cisplatin sensitivity of osteosarcoma cells in vitro through up-regulation of c-Myc and Bim signal. Cisplatin 18-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 96-101 29098029-7 2017 The results revealed that 5F and cisplatin synergistically induced apoptosis and inhibited cell growth, arrested cell cycles in the G0/G1 phase, downregulated beta-catenin, c-Myc and cyclin D1, and upregulated GSK-3beta. Cisplatin 33-42 MYC proto-oncogene, bHLH transcription factor Homo sapiens 173-178 29060932-7 2017 RESULTS: Treatment of U2OS cells with cisplatin induced cell apoptosis by upregulation of c-Myc -dependent Bim expression; Osteosarcoma U2OS cells transfected with miR-34a mimics (miR-34a/U2OS) induced cell apoptosis and inhibited cell survival, and increased the sensitivity of U2OS cells to cisplatin. Cisplatin 38-47 MYC proto-oncogene, bHLH transcription factor Homo sapiens 90-95 29060932-11 2017 CONCLUSIONS: Our data indicated that miR-34a enhanced the sensitivity to cisplatin by upregulation of c-Myc and Bim pathway. Cisplatin 73-82 MYC proto-oncogene, bHLH transcription factor Homo sapiens 102-107 28817737-9 2017 Myc/MDA-468 cells were resistant to standard chemotherapeutic treatments such as iniparib (PARP inhibitor) plus cisplatin, / iniparib, cisplatin, paclitaxel and docetaxel. Cisplatin 112-121 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3 29254192-11 2017 Additionally, inhibition of c-Myc enhanced cisplatin sensitivities in CCDC69 knockout A2780cis cells, overexpression of c-Myc reduced apoptosis in CCDC69 knockout SKOV3 cells. Cisplatin 43-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 28878262-0 2017 Hyper-O-GlcNAcylation induces cisplatin resistance via regulation of p53 and c-Myc in human lung carcinoma. Cisplatin 30-39 MYC proto-oncogene, bHLH transcription factor Homo sapiens 77-82 28878262-7 2017 Gene manipulation studies revealed that O-GlcNAcylation of p53/c-Myc is in part a regulator of CDDP-induced apoptosis. Cisplatin 95-99 MYC proto-oncogene, bHLH transcription factor Homo sapiens 63-68 28878262-8 2017 Accordingly, we classified CDDP resistance by hyper-O-GlcNAcylation in lung carcinoma cells as either p53 or c-Myc dependence based on their molecular targets. Cisplatin 27-31 MYC proto-oncogene, bHLH transcription factor Homo sapiens 109-114 28817737-9 2017 Myc/MDA-468 cells were resistant to standard chemotherapeutic treatments such as iniparib (PARP inhibitor) plus cisplatin, / iniparib, cisplatin, paclitaxel and docetaxel. Cisplatin 135-144 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3 28817737-10 2017 However, Myc/MDA-231 cells, which showed EMT changes responded to iniparib with cisplatin, but were resistant to other drugs, such as iniparib, cisplatin, paclitaxel and docetaxel. Cisplatin 80-89 MYC proto-oncogene, bHLH transcription factor Homo sapiens 9-12 28817737-10 2017 However, Myc/MDA-231 cells, which showed EMT changes responded to iniparib with cisplatin, but were resistant to other drugs, such as iniparib, cisplatin, paclitaxel and docetaxel. Cisplatin 144-153 MYC proto-oncogene, bHLH transcription factor Homo sapiens 9-12 28076844-6 2017 Experiments with nude mice carrying xenograft tumors showed that SFN sensitized NSCLC cells to cisplatin"s efficacy, which is accompanied by inhibition of cisplatin-induced c-MYC accumulation in tumor tissues. Cisplatin 95-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 173-178 28590415-5 2017 Paradoxically, oncogenic MYC can also promote the resistance of cancer cells to chemotherapeutic DNA-damaging agents such as cisplatin, clearly implying an antagonistic role of MYC in genomic instability. Cisplatin 125-134 MYC proto-oncogene, bHLH transcription factor Homo sapiens 25-28 29029460-0 2017 VRK1 promotes cisplatin resistance by up-regulating c-MYC via c-Jun activation and serves as a therapeutic target in esophageal squamous cell carcinoma. Cisplatin 14-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 52-57 29029460-11 2017 Silencing c-MYC abolished the c-Jun-mediated CDDP resistance of ESCC cells. Cisplatin 45-49 MYC proto-oncogene, bHLH transcription factor Homo sapiens 10-15 29029460-14 2017 Collectively, we conclude that VRK1 promotes CDDP resistance through c-MYC by activating c-Jun and potentiating a malignant phenotype in ESCC. Cisplatin 45-49 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-74 28623290-4 2017 TCRP1 upregulation in multidrug resistant tongue cancer cells (Tca8113/PYM) and cisplatin-resistant A549 lung cancer cells (A549/DDP) was accompanied by c-Myc upregulation, compared to respective parental cells. Cisplatin 80-89 MYC proto-oncogene, bHLH transcription factor Homo sapiens 153-158 28076844-6 2017 Experiments with nude mice carrying xenograft tumors showed that SFN sensitized NSCLC cells to cisplatin"s efficacy, which is accompanied by inhibition of cisplatin-induced c-MYC accumulation in tumor tissues. Cisplatin 155-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 173-178 27765932-0 2016 Cisplatin-induced synthetic lethality to arginine-starvation therapy by transcriptional suppression of ASS1 is regulated by DEC1, HIF-1alpha, and c-Myc transcription network and is independent of ASS1 promoter DNA methylation. Cisplatin 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 146-151 27765932-5 2016 We report here that cisplatin supppresses ASS1 expression is due to upregulation of HIF-1alpha and downregulation of c-Myc, which function as negative and positive regulators of ASS1 expression, respectively, by reciprocal bindings to the ASS1 promoter. Cisplatin 20-29 MYC proto-oncogene, bHLH transcription factor Homo sapiens 117-122 27492148-7 2016 High levels of mTOR, HIF-1alpha, c-Myc, and PKM2 were associated with a positive chemotherapy response in cervical cancer patients treated with cisplatin-based NACT. Cisplatin 144-153 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38 25411027-0 2015 Sequential treatment with aurora B inhibitors enhances cisplatin-mediated apoptosis via c-Myc. Cisplatin 55-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 88-93 26392091-4 2016 The analysis of the changes in the expression of genes involved in the response to DNA damage (CDKN1A, GADD45A, MDM2), apoptosis (BAX, BCL2) and oncogenesis (MYC, JUN) showed that 5-FU, CDDP and ET upregulated the genes involved in DNA damage response, while the anti-apoptotic gene BCL2 and oncogene MYC were downregulated. Cisplatin 186-190 MYC proto-oncogene, bHLH transcription factor Homo sapiens 158-161 27110775-7 2016 Smad3 upregulated p21(Waf1/Cip1) and downregulated c-myc and bcl2 with the treatment of cisplatin. Cisplatin 88-97 MYC proto-oncogene, bHLH transcription factor Homo sapiens 51-56 26227489-1 2015 The purpose of this study was to investigate the molecular and therapeutic effects of siRNA-mediated c-MYC silencing in cisplatin-resistant ovarian cancer. Cisplatin 120-129 MYC proto-oncogene, bHLH transcription factor Homo sapiens 101-106 26227489-3 2015 Furthermore, analysis of a panel of ovarian cancer cell lines showed that c-MYC protein levels were higher in cisplatin-resistant cells when compared with their cisplatin-sensitive counterparts. Cisplatin 110-119 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-79 26227489-3 2015 Furthermore, analysis of a panel of ovarian cancer cell lines showed that c-MYC protein levels were higher in cisplatin-resistant cells when compared with their cisplatin-sensitive counterparts. Cisplatin 161-170 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-79 26227489-4 2015 In vitro cell viability, growth, cell-cycle progression, and apoptosis, as well as in vivo therapeutic effectiveness in murine xenograft models, were also assessed following siRNA-mediated c-MYC silencing in cisplatin-resistant ovarian cancer cells. Cisplatin 208-217 MYC proto-oncogene, bHLH transcription factor Homo sapiens 189-194 25411027-11 2015 c-Myc-dependent induction of polyploidy sensitizes cells to cisplatin. Cisplatin 60-69 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 25411027-7 2015 Thus, our report reveals for the first time that sequential treatment of Aurora B inhibitors and cisplatin is essential to inhibit ovarian carcinoma by inducing polyploidy and downregulating c-Myc and that c-Myc is identified as a predictive biomarker to select cells responsive to chemotherapeutical combinations targeting Aurora B. Cisplatin 97-106 MYC proto-oncogene, bHLH transcription factor Homo sapiens 191-196 25411027-7 2015 Thus, our report reveals for the first time that sequential treatment of Aurora B inhibitors and cisplatin is essential to inhibit ovarian carcinoma by inducing polyploidy and downregulating c-Myc and that c-Myc is identified as a predictive biomarker to select cells responsive to chemotherapeutical combinations targeting Aurora B. Cisplatin 97-106 MYC proto-oncogene, bHLH transcription factor Homo sapiens 206-211 25411027-10 2015 The synergy of Aurora B inhibitor with cisplatin is dependent on c-Myc expression. Cisplatin 39-48 MYC proto-oncogene, bHLH transcription factor Homo sapiens 65-70 25796504-0 2015 Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin. Cisplatin 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24 25796504-0 2015 Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin. Cisplatin 238-247 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24 25796504-6 2015 Moreover, cisplatin increased the expression of c-myc in the presence of TRAIL, and there is a clear increase in cyt c release from mitochondria with the increasing concentrations of cisplatin. Cisplatin 10-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 48-53 25748238-0 2015 Erlotinib-cisplatin combination inhibits growth and angiogenesis through c-MYC and HIF-1alpha in EGFR-mutated lung cancer in vitro and in vivo. Cisplatin 10-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 73-78 25796504-8 2015 Together, we conclude that in TRAIL-treated MDR gastric carcinoma cells, cisplatin induces the death receptors DR4 and DR5 through the up-regulation of c-myc and strengthens the activation of caspases via promoting the release of cyt c. Cisplatin 73-82 MYC proto-oncogene, bHLH transcription factor Homo sapiens 152-157 25748238-9 2015 These results suggest that low dose erlotinib-cisplatin combination exhibits its anti-tumor activity by targeting angiogenesis through the modulation of the c-MYC/HIF-1alpha/VEGF pathway in NSCLC with EGFR exon 19 deletions. Cisplatin 46-55 MYC proto-oncogene, bHLH transcription factor Homo sapiens 157-162 18375382-5 2008 Under conditions when the expression of endogenous c-Myc, caspase-2, or Apaf-1 is reduced 80-90%, cisplatin (or etoposide)-induced apoptosis is significantly decreased. Cisplatin 98-107 MYC proto-oncogene, bHLH transcription factor Homo sapiens 51-56 24926545-9 2014 C-MYC and PVT1 knockdown reduced cell proliferation and increased sensitivity to cisplatin. Cisplatin 81-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 23879689-10 2013 Heat-induced increase in Ctr1 multimerisation with cisplatin was observed in Myc-tagged Ctr1 cells. Cisplatin 51-60 MYC proto-oncogene, bHLH transcription factor Homo sapiens 77-80 23225459-6 2012 On the other hand, those with c-MYC-positive expression tended to have a worse prognosis and were resistant to cisplatin-based chemotherapy. Cisplatin 111-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 30-35 22778941-4 2012 In addition, a new mechanism has recently been revealed, in which the oncoprotein c-Myc suppresses bridging integrator 1 (BIN1), thereby releasing poly(ADP-ribose)polymerase 1, which results in increased DNA repair activity and allows cancer cells to acquire cisplatin resistance. Cisplatin 259-268 MYC proto-oncogene, bHLH transcription factor Homo sapiens 82-87 21447800-0 2011 c-MYC suppresses BIN1 to release poly(ADP-ribose) polymerase 1: a mechanism by which cancer cells acquire cisplatin resistance. Cisplatin 106-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 21447800-2 2011 We show that the c-MYC oncoprotein increases cisplatin resistance by decreasing production of the c-MYC inhibitor BIN1 (bridging integrator 1). Cisplatin 45-54 MYC proto-oncogene, bHLH transcription factor Homo sapiens 17-22 21447800-2 2011 We show that the c-MYC oncoprotein increases cisplatin resistance by decreasing production of the c-MYC inhibitor BIN1 (bridging integrator 1). Cisplatin 45-54 MYC proto-oncogene, bHLH transcription factor Homo sapiens 98-103 21447800-7 2011 Thus, a c-MYC-mediated positive feedback loop may contribute to cancer cell resistance to cisplatin. Cisplatin 90-99 MYC proto-oncogene, bHLH transcription factor Homo sapiens 8-13 20890087-5 2010 Furthermore, downregulation of c-Myc effectively overcame Aurora-A-induced resistance to cisplatin in esophageal cancer cells. Cisplatin 89-98 MYC proto-oncogene, bHLH transcription factor Homo sapiens 31-36 19996588-0 2009 Enhancement effect of adenovirus-mediated antisense c-myc and caffeine on the cytotoxicity of cisplatin in osteosarcoma cell lines. Cisplatin 94-103 MYC proto-oncogene, bHLH transcription factor Homo sapiens 52-57 19996588-9 2009 Myc-AS or caffeine can enhance the cytotoxic effects of 2.0 and 5.0 microg/ml CDDP on MG-63 cells. Cisplatin 78-82 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3 19996588-10 2009 Moreover, the significantly enhancing effect of the Myc-AS-caffeine combination on CDDP chemotherapy of MG-63 cells was not restricted to apoptosis but also decreased tumor cell proliferation in vitro. Cisplatin 83-87 MYC proto-oncogene, bHLH transcription factor Homo sapiens 52-55 19996588-14 2009 Myc-AS combined with caffeine can enhance apoptosis induction and chemotherapeutic effects of CDDP on osteosarcoma MG-63 cells. Cisplatin 94-98 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3 19054066-2 2009 The telomeric regions of DNA and nuclease hypersensitive elements of human c-myc and PDGF-A promoters represent a very appealing target for cisplatin and may interfere with normal DNA function. Cisplatin 140-149 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-80 25131138-3 2014 beta-Catenin and c-Myc protein expression following cisplatin treatment were determined using western blotting and immunofluorescence. Cisplatin 52-61 MYC proto-oncogene, bHLH transcription factor Homo sapiens 17-22 25131138-6 2014 Endogenous beta-catenin and c-Myc expression in A549/DDP cells were higher than that in A549 cells, and were upregulated in A549/DDP cells (p < 0.05) and downregulated in A549 cells after 48 h cisplatin treatment (p < 0.05). Cisplatin 196-205 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 25131138-7 2014 beta-catenin localization transferred from membrane/cytoplasmic/nuclear to cytoplasmic/nuclear, and c-Myc localization transferred from cytoplasmic/nuclear to nuclear in both cell lines following cisplatin treatment. Cisplatin 196-205 MYC proto-oncogene, bHLH transcription factor Homo sapiens 100-105 25131138-11 2014 C-myc, the downstream target gene of beta-catenin, plays an important role in regulating cisplatin resistance in A549/DDP cells. Cisplatin 89-98 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 25131138-12 2014 C-Myc siRNA improved the sensitivity of A549/DDP cells to cisplatin. Cisplatin 58-67 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 23685757-7 2013 At a concentration of 5.0 microg/ml CDDP, the growth inhibition rates were 53.3+-5.2, 42.7+-6.3 and 40.9+-4.7% in the combined, c-myc and Bmi-1 siRNA groups, respectively. Cisplatin 36-40 MYC proto-oncogene, bHLH transcription factor Homo sapiens 128-133 21324178-4 2011 RESULTS: In DAOY - and to a lesser extent in UW228 - cells expressing high levels of c-MYC, the cytotoxicity of cisplatin, and etoposide was significantly higher when compared with DAOY/UW228 cells expressing low levels of c-MYC. Cisplatin 112-121 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-90 21324178-4 2011 RESULTS: In DAOY - and to a lesser extent in UW228 - cells expressing high levels of c-MYC, the cytotoxicity of cisplatin, and etoposide was significantly higher when compared with DAOY/UW228 cells expressing low levels of c-MYC. Cisplatin 112-121 MYC proto-oncogene, bHLH transcription factor Homo sapiens 223-228 20459793-0 2010 Kaempferol enhances cisplatin"s effect on ovarian cancer cells through promoting apoptosis caused by down regulation of cMyc. Cisplatin 20-29 MYC proto-oncogene, bHLH transcription factor Homo sapiens 120-124 20459793-10 2010 However, significant inhibition of ABCC6 and cMyc mRNA levels was observed for the cisplatin/kaempferol combined treatment. Cisplatin 83-92 MYC proto-oncogene, bHLH transcription factor Homo sapiens 45-49 20459793-15 2010 CONCLUSIONS: Kaempferol enhances the effect of cisplatin through down regulation of cMyc in promoting apoptosis of ovarian cancer cells. Cisplatin 47-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 84-88 20008890-0 2010 c-MYC depletion potentiates cisplatin-induced apoptosis in head and neck squamous cell carcinoma: involvement of TSP-1 up-regulation. Cisplatin 28-37 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 19134217-7 2009 On the other hand, down-regulation of c-MYC reduced apoptosis and decreased the sensitivity of human MB cells to IR, cisplatin, and etoposide. Cisplatin 117-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 38-43 17473215-4 2007 Cell viability after cisplatin treatment of c-myc-overexpressing, control, and siRNA-transfected cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and drug-induced apoptosis was measured by DNA fragmentation, sub-G(1), and poly(ADP-ribose) polymerase cleavage analyses. Cisplatin 21-30 MYC proto-oncogene, bHLH transcription factor Homo sapiens 44-49 17628013-2 2007 We found that specific c-Myc inhibition depleted cells of GSH by directly reducing the gene expression of both heavy and light subunits of the gamma-GCS enzyme and increased their susceptibility to antineoplastic drugs with different mechanisms of action, such as cisplatin (CDDP), staurosporine (STR), and 5-fluorouracil (5-FU). Cisplatin 264-273 MYC proto-oncogene, bHLH transcription factor Homo sapiens 23-28 17628013-2 2007 We found that specific c-Myc inhibition depleted cells of GSH by directly reducing the gene expression of both heavy and light subunits of the gamma-GCS enzyme and increased their susceptibility to antineoplastic drugs with different mechanisms of action, such as cisplatin (CDDP), staurosporine (STR), and 5-fluorouracil (5-FU). Cisplatin 275-279 MYC proto-oncogene, bHLH transcription factor Homo sapiens 23-28 17628013-3 2007 The effect caused by c-Myc inhibition on CDDP and STR response, but not to 5-FU treatment, is directly linked to the impairment of the gamma-GCS expression, because up-regulation of gamma-GCS reverted drug sensitivity, whereas the interference of GSH synthesis increased drug susceptibility as much as after c-Myc down-regulation. Cisplatin 41-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 21-26 17628013-5 2007 Indeed, although 5-FU exposure did not induce any ROS, CDDP- and STR-induced oxidative stress enhanced the recruitment of c-Myc on both gamma-GCS promoters, thus stimulating GSH neosynthesis and allowing cells to recover from ROS-induced drug damage. Cisplatin 55-59 MYC proto-oncogene, bHLH transcription factor Homo sapiens 122-127 17473215-6 2007 RESULTS: Ectopic overexpression of c-myc in murine and human pancreatic cancer cell lines, Ela-myc and L3.6pl, respectively, resulted in increased sensitivity to cisplatin and other chemotherapeutic drugs. Cisplatin 162-171 MYC proto-oncogene, bHLH transcription factor Homo sapiens 35-40 17473215-7 2007 Increased sensitivity to cisplatin in c-myc-overexpressing cells was due, in part, to the marked increase in cisplatin-induced apoptosis. Cisplatin 25-34 MYC proto-oncogene, bHLH transcription factor Homo sapiens 38-43 17473215-7 2007 Increased sensitivity to cisplatin in c-myc-overexpressing cells was due, in part, to the marked increase in cisplatin-induced apoptosis. Cisplatin 109-118 MYC proto-oncogene, bHLH transcription factor Homo sapiens 38-43 17473215-8 2007 Conversely, down-regulation of c-myc expression in stable c-myc-overexpressing cells by c-myc siRNA resulted in decreased sensitivity to cisplatin-induced cell death. Cisplatin 137-146 MYC proto-oncogene, bHLH transcription factor Homo sapiens 31-36 17473215-8 2007 Conversely, down-regulation of c-myc expression in stable c-myc-overexpressing cells by c-myc siRNA resulted in decreased sensitivity to cisplatin-induced cell death. Cisplatin 137-146 MYC proto-oncogene, bHLH transcription factor Homo sapiens 58-63 17473215-8 2007 Conversely, down-regulation of c-myc expression in stable c-myc-overexpressing cells by c-myc siRNA resulted in decreased sensitivity to cisplatin-induced cell death. Cisplatin 137-146 MYC proto-oncogene, bHLH transcription factor Homo sapiens 58-63 17473215-10 2007 The c-myc-induced cisplatin sensitivity correlated with inhibition of nuclear factor kappaB activity, which was partially restored by ectopic cyclin D1 overexpression. Cisplatin 18-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9 16681749-4 2006 In total, 21 protein spots were found to be differentially expressed following cisplatin treatment, of which 12 were upregulated (eg, regulator of G-protein signaling, TRAF:TNF (tumor necrosis factor) receptor-associated factor-interacting protein [I-TRAF], and cyclin-dependent kinase inhibitor p27 [p27(kip1)]) and 9 were downregulated (eg, myc proto-oncoprotein [c-myc] and proliferating cell nuclear antigen). Cisplatin 79-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 366-371 16788862-5 2006 Furthermore, c-Myc expression repressed the activation of Akt induced by the toxic agents doxorubicin, cisplatin and H(2)O(2), and also by the physiological agonists PDGF and insulin. Cisplatin 103-112 MYC proto-oncogene, bHLH transcription factor Homo sapiens 13-18 16083584-0 2005 [Adenovirus mediated antisense c-myc gene on the chemotherapy sensitivity of osteosarcoma cells to cisplatin]. Cisplatin 99-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 31-36 16466985-0 2006 Recombinant antisense C-myc adenovirus increase in vitro sensitivity of osteosarcoma MG-63 cells to cisplatin. Cisplatin 100-109 MYC proto-oncogene, bHLH transcription factor Homo sapiens 22-27 16466985-8 2006 Ad-Asc-myc downregulated the expression of c-myc protein after transfected MG-63 cells for 48 hours, combined with the treatment of 2.0, 5.0 microg/ml cisplatin for 2 hours can inhibited tumor cells proliferation in vitro by 33.4 and 54.2 percent, respectively, which had significant difference compared with control recombinant adenovirus (Ad-LacZ) groups (P < 0.05). Cisplatin 151-160 MYC proto-oncogene, bHLH transcription factor Homo sapiens 5-10 16466985-10 2006 Detection of caspase-3 protein TEM, and FCM analysis showed that Ad-Asc-myc could induce apoptosis of transfected cells, which was enhanced by the treatment of cisplatin. Cisplatin 160-169 MYC proto-oncogene, bHLH transcription factor Homo sapiens 72-75 16466985-12 2006 In conclusion, Ad-Asc-myc increased the in vitro sensitivity of osteosarcoma MG-63 cells to cisplatin as well as induced apoptosis. Cisplatin 92-101 MYC proto-oncogene, bHLH transcription factor Homo sapiens 22-25 16083584-1 2005 OBJECTIVE: To construct the recombinant adenovirus encoding antisense c-myc fragment and to investigate its effect on the chemotherapy sensitivity of osteosarcoma MG-63 cells to cisplatin. Cisplatin 178-187 MYC proto-oncogene, bHLH transcription factor Homo sapiens 70-75 16083584-5 2005 Ad-Asc-myc down-regulated the expression of c-myc protein after transfected MG-63 cells for 48 h, combined with the treatment of 2.0, 5.0 microg/ml cisplatin for 2 h could inhibit tumor cells proliferation in vitro by 33.4% and 54.2% respectively, which were significantly difference compared with control recombinant adenovirus (Ad-LacZ) groups (P < 0.05). Cisplatin 148-157 MYC proto-oncogene, bHLH transcription factor Homo sapiens 7-10 16083584-5 2005 Ad-Asc-myc down-regulated the expression of c-myc protein after transfected MG-63 cells for 48 h, combined with the treatment of 2.0, 5.0 microg/ml cisplatin for 2 h could inhibit tumor cells proliferation in vitro by 33.4% and 54.2% respectively, which were significantly difference compared with control recombinant adenovirus (Ad-LacZ) groups (P < 0.05). Cisplatin 148-157 MYC proto-oncogene, bHLH transcription factor Homo sapiens 5-10 16083584-6 2005 Acridine Orange staining and FCM analysis showed that Ad-Asc-myc could induce apoptosis of transfected cells, which was enhanced by the treatment of cisplatin cell. Cisplatin 149-158 MYC proto-oncogene, bHLH transcription factor Homo sapiens 61-64 16083584-8 2005 CONCLUSION: Ad-Asc-myc increases the chemotherapy sensitivity of osteosarcoma MG-63 cells to cisplatin as well as induced apoptosis. Cisplatin 93-102 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-22 11408612-0 2001 c-Myc down-regulation increases susceptibility to cisplatin through reactive oxygen species-mediated apoptosis in M14 human melanoma cells. Cisplatin 50-59 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 12435808-2 2002 In this study, we show that c-Myc expression is induced by many cellular insults, including cisplatin, doxorubicin, paclitaxel, 5-flourouracil, H(2)O(2), and radiation, and the enhanced expression of c-Myc protects against cell death caused by these cellular insults through ornithine decarboxylase (ODC) induction. Cisplatin 92-101 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 12435808-4 2002 We also found that cisplatin activated nuclear factor-kappaB, and this subsequently induced c-Myc expression, resulting in the blocking of apoptosis through ODC induction. Cisplatin 19-28 MYC proto-oncogene, bHLH transcription factor Homo sapiens 92-97 12123658-6 2002 Both VM-26 (1-10 microM) and cisplatin (25-100 microM) induced a dose-dependent decrease in the amount of intact c-myc sequence. Cisplatin 29-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 113-118 15720258-5 2005 It is known that the tumor-suppressor proteins p53 and p73, and the oncoprotein c-Myc, which function as transcription factors, influence cellular sensitivity to cisplatin. Cisplatin 162-171 MYC proto-oncogene, bHLH transcription factor Homo sapiens 80-85 15153331-2 2004 By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc antisense transfectants, but not in the parental line. Cisplatin 95-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 27-32 15153331-2 2004 By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc antisense transfectants, but not in the parental line. Cisplatin 95-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150 12080043-6 2002 In turn, c-Myc transactivated an intact YB-1 promoter but not a YB-1 promoter with a mutant E-box, indicating that the E-box is necessary for the response of the promoter to cisplatin. Cisplatin 174-183 MYC proto-oncogene, bHLH transcription factor Homo sapiens 9-14 11707650-0 2001 Modification of the sensitivity to cisplatin with c-myc over-expression or down-regulation in colon cancer cells. Cisplatin 35-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 50-55 11707650-2 2001 On the other hand, SW480DDP cell lines resistant to cisplatin exhibited decreased c-myc gene expression, but their cell growth rates remained similar to those of their parental cells. Cisplatin 52-61 MYC proto-oncogene, bHLH transcription factor Homo sapiens 82-87 11707650-3 2001 Antisense oligonucleotides to c-myc inhibited c-myc expression and induced increased resistance to cisplatin in SW480 cells. Cisplatin 99-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 30-35 11707650-4 2001 In contrast, SW480DDP cells showed increased c-myc expression and reversed sensitivity to cisplatin when these cells were transfected with c-myc cDNA from the pLNCX plasmid. Cisplatin 90-99 MYC proto-oncogene, bHLH transcription factor Homo sapiens 139-144 11707650-5 2001 Moreover, SW480DDP cells transfected with c-myc cDNA induced apoptosis when exposed to cisplatin, but not SW480 cells transfected with an antisense sequence for c-myc. Cisplatin 87-96 MYC proto-oncogene, bHLH transcription factor Homo sapiens 42-47 11707650-7 2001 Thus enforced expression of c-myc in SW480 and SW620 lines sensitizes cells to cisplatin-induced apoptosis, whereas the down-regulation of c-myc in SW480DDP and SW620DDP increases cisplatin resistance when using antisense strategy. Cisplatin 79-88 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 11707650-7 2001 Thus enforced expression of c-myc in SW480 and SW620 lines sensitizes cells to cisplatin-induced apoptosis, whereas the down-regulation of c-myc in SW480DDP and SW620DDP increases cisplatin resistance when using antisense strategy. Cisplatin 180-189 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 11408612-1 2001 Our aim in this work was to define the role of c-Myc in the susceptibility to cisplatin [cis-diamminedichloroplatinum(II) (CDDP)] in human melanoma cells. Cisplatin 78-87 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 11408612-1 2001 Our aim in this work was to define the role of c-Myc in the susceptibility to cisplatin [cis-diamminedichloroplatinum(II) (CDDP)] in human melanoma cells. Cisplatin 89-121 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 11408612-1 2001 Our aim in this work was to define the role of c-Myc in the susceptibility to cisplatin [cis-diamminedichloroplatinum(II) (CDDP)] in human melanoma cells. Cisplatin 123-127 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 11408612-3 2001 Analysis of survival curves demonstrates an increase in CDDP sensitivity in c-Myc low-expressing clones if compared with the control clone and the parental line. Cisplatin 56-60 MYC proto-oncogene, bHLH transcription factor Homo sapiens 76-81 11408612-7 2001 The use of the antioxidant N-acetyl cysteine and caspase inhibitors prevents CDDP-induced apoptosis in c-Myc low-expressing clones, demonstrating that ROS, caspase-1, and caspase-3 are required for apoptotic cell death. Cisplatin 77-81 MYC proto-oncogene, bHLH transcription factor Homo sapiens 103-108 11408612-8 2001 Moreover, ROS generation depends on caspase-1-like activation because the Ac-YVAD-cho inhibitor abrogates CDDP-induced ROS in the c-Myc low-expressing clones. Cisplatin 106-110 MYC proto-oncogene, bHLH transcription factor Homo sapiens 130-135 9443406-0 1998 c-myc antisense oligodeoxynucleotides enhance the efficacy of cisplatin in melanoma chemotherapy in vitro and in nude mice. Cisplatin 62-71 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 10499637-0 1999 Increase of cisplatin sensitivity by c-myc antisense oligodeoxynucleotides in a human metastatic melanoma inherently resistant to cisplatin. Cisplatin 12-21 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-42 10499637-0 1999 Increase of cisplatin sensitivity by c-myc antisense oligodeoxynucleotides in a human metastatic melanoma inherently resistant to cisplatin. Cisplatin 130-139 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-42 10499637-1 1999 In this study, we evaluated the role of the c-myc oncogene in response to cisplatin (DDP) treatment using two melanoma lines derived from the primary tumor (LP) and metastatic lymph node (LM) of the same patient. Cisplatin 74-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 44-49 9443406-1 1998 This study was designed to assess the efficacy of a new antimelanoma therapeutic strategy that relies on the use of a c-myc antisense 15-mer phosphorothioate oligodeoxynucleotide ([S]ODN), in combination with cisplatin (cis-diamminedichloroplatinum; DDP), which is currently used in the clinical management of melanoma patients. Cisplatin 209-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 118-123 9443406-1 1998 This study was designed to assess the efficacy of a new antimelanoma therapeutic strategy that relies on the use of a c-myc antisense 15-mer phosphorothioate oligodeoxynucleotide ([S]ODN), in combination with cisplatin (cis-diamminedichloroplatinum; DDP), which is currently used in the clinical management of melanoma patients. Cisplatin 220-248 MYC proto-oncogene, bHLH transcription factor Homo sapiens 118-123 9389570-4 1997 We studied the existence of a correlation between resistance and activation of the c-myc oncogene in a cDDP-resistant SCLC sub-line, GLC4cDDP, containing a c-myc gene amplification. Cisplatin 103-107 MYC proto-oncogene, bHLH transcription factor Homo sapiens 83-88 9389570-4 1997 We studied the existence of a correlation between resistance and activation of the c-myc oncogene in a cDDP-resistant SCLC sub-line, GLC4cDDP, containing a c-myc gene amplification. Cisplatin 103-107 MYC proto-oncogene, bHLH transcription factor Homo sapiens 156-161 9389570-10 1997 Furthermore, AS-c-myc RNA expression caused a 1.4-fold increased cDDP sensitivity but no change in doxorubicin or vincristine sensitivity in GLC4cDDP/AS cells. Cisplatin 65-69 MYC proto-oncogene, bHLH transcription factor Homo sapiens 16-21 9389570-11 1997 Our results indicate that AS-c-myc RNA expression causes inhibition of cell proliferation, induces apoptosis, reduces clonogenicity and interferes with cDDP sensitivity but not with doxorubicin or vincristine sensitivity. Cisplatin 152-156 MYC proto-oncogene, bHLH transcription factor Homo sapiens 29-34