PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 1540946-4 1992 When c-myc levels and responses to serum induction were analyzed in the presence of inducers of differentiation, i.e., dimethylformamide, retinoic acid, sodium butyrate and TGF-beta, distinct patterns of sensitivity and resistance emerged. Tretinoin 138-151 MYC proto-oncogene, bHLH transcription factor Homo sapiens 5-10 2163931-2 1990 Induction of c-fos transcripts was not observed at times early or late during retinoic acid-promoted differentiation, but a decrease in c-myc mRNA was noted as early as 1 h after retinoic acid dosing. Tretinoin 179-192 MYC proto-oncogene, bHLH transcription factor Homo sapiens 136-141 2201551-2 1990 In HL-R5 cells, resistant to the induction of differentiation by retinoic acid but not DMSO, the characteristic c-myc down-regulation which is associated with HL-60 differentiation, as well as increased levels of MRP8 and MRP14, is detectable only after DMSO treatment. Tretinoin 65-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 112-117 3180083-0 1988 Changes in c-myc, c-fms, and N-ras proto-oncogene expression associated with retinoic acid-induced monocytic differentiation of human leukemia HL60/MRI cells. Tretinoin 77-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 11-16 34236140-0 2021 All-trans retinoic acid induces leukemia resistance to NK cell cytotoxicity by down-regulating B7-H6 expression via c-Myc signaling. Tretinoin 3-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 116-121 34236140-6 2021 We used CRISPR/Cas9 to knockdown B7-H6 expression and siRNA to knockdown c-Myc in U-937 cells to evaluate the role of B7-H6 and c-Myc in atRA-induced tumor resistance against NK cells. Tretinoin 137-141 MYC proto-oncogene, bHLH transcription factor Homo sapiens 128-133 35468223-4 2022 We find that ATRA treatment in combination with inhibition of PI3K (ZSTK474), mTOR (WYE132) or PI3K/mTOR (BEZ235, dactolisib) drastically reduces protein levels of the proto-oncogene MYC. Tretinoin 13-17 MYC proto-oncogene, bHLH transcription factor Homo sapiens 183-186 2555051-5 1989 Retinoic acid incubation caused a reproducible decrease in c-myc expression in variant SCLC cells, but was not noted to increase L-dopa decarboxylase, an enzyme which biochemically distinguishes classic from variant SCLC cell lines. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 59-64 34236140-11 2021 On the other hand, atRA treatment reduced c-Myc expression, which in turn inhibited the transcription of B7-H6 on leukemia cells. Tretinoin 19-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 42-47 34236140-12 2021 CONCLUSION: atRA treatment promotes tumor cell resistance against NK cell-mediated lysis by down-regulating B7-H6 expression via the c-Myc signaling pathway, suggesting that more attention needs to be paid to the immunological adverse effects in the clinical use of atRA treatment. Tretinoin 12-16 MYC proto-oncogene, bHLH transcription factor Homo sapiens 133-138 35468223-5 2022 In combination with BEZ235, ATRA treatment led to almost complete eradication of cellular MYC, G1 arrest, loss of clonal capacity and terminal granulocytic differentiation. Tretinoin 28-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 90-93 35468223-6 2022 We demonstrate that PAM inhibitor/ATRA treatment targets MYC via independent mechanisms. Tretinoin 34-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 57-60 35468223-7 2022 While inhibition of the PAM pathway causes MYC phosphorylation at threonine 58 via glycogen synthase kinase 3 beta and subsequent degradation, ATRA reduces its expression. Tretinoin 143-147 MYC proto-oncogene, bHLH transcription factor Homo sapiens 43-46 3100942-0 1987 Synergistic effect of retinoic acid and calcium ionophore A23187 on differentiation, c-myc expression, and membrane tyrosine kinase activity in human promyelocytic leukemia cell line HL-60. Tretinoin 22-35 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-90 3164710-2 1988 In the present report, Northern analysis indicates that addition of the maturational agent N,N-dimethylformamide (DMF) (1.0%) to proliferating HCT 116 and MOSER cells resulted in a repression of c-myc proto-oncogene expression; retinoic acid (1.0 microM) was less effective in this regard. Tretinoin 228-241 MYC proto-oncogene, bHLH transcription factor Homo sapiens 195-200 2459072-0 1988 Retinoic-acid-induced modulation of c-myc not dependent on its continued presence: possible role in pre-commitment for HL-60 cells. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-41 2459072-7 1988 Thus, retinoic acid induced a change in HL-60 c-myc RNA levels which was sustained regardless of the continued presence or absence of RA. Tretinoin 6-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-51 3327864-1 1987 The quantity of c-myc mRNA was measured during the retinoic-acid-induced differentiation of the pluripotent human teratoma cell line, Tera-2 cl. Tretinoin 51-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 16-21 3100942-8 1987 Significantly greater reduction in c-myc mRNA levels was also observed 24 hr after treatment with RA and A23187 in comparison to that observed with either agent alone. Tretinoin 98-100 MYC proto-oncogene, bHLH transcription factor Homo sapiens 35-40 3100942-9 1987 These results suggest that a Ca2+-mediated process sensitizes cells to the differentiating effect of RA and that this effect is associated with a significant reduction of c-myc expression and the induction of membrane tyrosine kinase activity in this cell line. Tretinoin 101-103 MYC proto-oncogene, bHLH transcription factor Homo sapiens 171-176 3520340-3 1986 When the human promyelocytic leukaemia cell line HL60 is treated with retinoic acid, the cells differentiate into granulocytes, and there is a reduction in steady state c-myc RNA of more than 10-fold. Tretinoin 70-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 169-174 3325885-6 1987 In contrast, when the cells were exposed to retinoic acid, which results in a maturation along an alternative pathway, the inhibition of N-myc and c-myc expression was similar. Tretinoin 44-57 MYC proto-oncogene, bHLH transcription factor Homo sapiens 147-152 3460694-1 1986 The dynamics in levels of HL-60 (a human promyelocytic leukemia cell line) c-myc RNA due to retinoic acid-induced myeloid differentiation were measured. Tretinoin 92-105 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-80 3460694-8 1986 Since c-myc encodes a putative nuclear matrix protein, the results suggest a regulatory role for increased c-myc expression in mediating the nuclear structural change characteristic of precommitment early in the retinoic acid-induced process of HL-60 terminal myeloid differentiation. Tretinoin 212-225 MYC proto-oncogene, bHLH transcription factor Homo sapiens 107-112 3785153-0 1986 c-myc regulation during retinoic acid-induced differentiation of F9 cells is posttranscriptional and associated with growth arrest. Tretinoin 24-37 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 3785153-1 1986 We have shown that c-myc mRNA levels decrease more than 20-fold when F9 teratocarcinoma stem cells are induced to arrest growth and terminally differentiate to parietal endoderm after exposure to retinoic acid and cyclic AMP (Campisi et al., Cell 36:241-247, 1984). Tretinoin 196-209 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24 3785153-2 1986 Here, we demonstrate that although growth arrest and full expression of the differentiated phenotype required about 3 days, c-myc mRNA declined abruptly between 8 and 16 h after the addition of retinoic acid and cyclic AMP. Tretinoin 194-207 MYC proto-oncogene, bHLH transcription factor Homo sapiens 124-129 3785153-5 1986 Thus, decreased c-myc mRNA is a consequence of very early posttranscriptional regulation directed by retinoic acid. Tretinoin 101-114 MYC proto-oncogene, bHLH transcription factor Homo sapiens 16-21 3916193-3 1985 In particular, it is shown that retinoic acid inhibits the proliferative effects of transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF) on fibroblasts that have been transfected with the c-myc oncogene. Tretinoin 32-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 220-225 3916193-4 1985 The ability of retinoic acid to induce differentiation in several types of human and murine tumor cells also is associated with the ability of retinoic acid to suppress the expression of either the c-myc oncogene, or the related N-myc gene. Tretinoin 15-28 MYC proto-oncogene, bHLH transcription factor Homo sapiens 198-203 3916193-4 1985 The ability of retinoic acid to induce differentiation in several types of human and murine tumor cells also is associated with the ability of retinoic acid to suppress the expression of either the c-myc oncogene, or the related N-myc gene. Tretinoin 143-156 MYC proto-oncogene, bHLH transcription factor Homo sapiens 198-203 32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 49-72 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3 6424665-1 1984 A decrease in the expression of the myc proto-oncogene of HL-60 cells has been reported as an accompaniment of myeloid differentiation induced by either dimethylsulfoxide or retinoic acid. Tretinoin 174-187 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-39 32536235-6 2020 Further studies revealed that ATO/ATRA may suppress the Expression of FLT3-ITD by promoting the UBE2L6-mediated ubiquitination pathway and decreasing the expression of C-MYC. Tretinoin 34-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 168-173 32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 49-72 MYC proto-oncogene, bHLH transcription factor Homo sapiens 20-23 32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 74-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3 32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 74-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 20-23 27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 85-98 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-192 31264378-8 2019 Furthermore, we demonstrated that expressions of c-Myc and miR-17-92 are markedly suppressed during ATRA-induced NB4 cell differentiation. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 49-54 30123134-12 2018 In validating experiments, combination of Lapatinib and all-trans retinoic acid (ATRA) synergistically suppresses cell growth, and accompanied by decreased expression of MYC. Tretinoin 60-79 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-173 30123134-12 2018 In validating experiments, combination of Lapatinib and all-trans retinoic acid (ATRA) synergistically suppresses cell growth, and accompanied by decreased expression of MYC. Tretinoin 81-85 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-173 29699387-5 2018 In this study, we investigated the combined effect of ATRA and bromodomain inhibitor JQ1, proven to have potent anti-cancer activity mainly through inhibition of c-Myc. Tretinoin 54-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 162-167 27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-192 25127121-3 2014 c-Myc over-expression in leukemic cells induced resistance to chemotherapeutic drugs, enhanced colony formation capacity and inhibited cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 177-190 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 27182202-10 2016 Augmented downregulation of c-Myc protein expression was observed in the combination treatment with ATRA, VD3 and dasatinib compared to treatment with each reagent alone in HL-60 cells. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 26248086-10 2015 Genes in a pathway regulated by retinoic acid-regulated nuclear protein made the largest contribution to this gene set (P < .0001); the transcription factor MYC regulated at least 30% of genes within the signature (P < .0001). Tretinoin 32-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 160-163 26545364-6 2015 We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. Tretinoin 78-91 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-40 26545364-6 2015 We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. Tretinoin 93-97 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-40 25127121-3 2014 c-Myc over-expression in leukemic cells induced resistance to chemotherapeutic drugs, enhanced colony formation capacity and inhibited cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 192-196 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 24646031-9 2014 Finally, sharp reduction in c-Myc has been observed in several leukaemia cell lines treated with ATRA, which may regulate expression of CDKs and CKIs. Tretinoin 97-101 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33 25072246-3 2014 Real-time PCR analyses demonstrated that the inductions of CD11b and CD11c and reductions in myeloperoxidase and c-myc by ATRA were significantly attenuated in NB4MTOE cells. Tretinoin 122-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 113-118 23528537-6 2013 Upon RA treatment, c-Myc is quickly degraded via the proteasome-dependent pathway. Tretinoin 5-7 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24 23562609-7 2013 During SIRPalpha induction, levels of these 3 miRNAs were all reduced, and their downregulation by retinoic acid or phorbol 12-myristate 13-acetate occurred through suppression of the c-Myc signaling pathway. Tretinoin 99-112 MYC proto-oncogene, bHLH transcription factor Homo sapiens 184-189 24516348-13 2014 The transcription and translation of C-MYC was detected in HL-60/pAd-NLS-RARalpha cells which treated by ATRA. Tretinoin 105-109 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-42 24516348-17 2014 The expression of C-MYC increased strikingly in HL-60/pAd-NLS-RARalpha cells treated with 2.5micromol/L ATRA. Tretinoin 104-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23 23588859-0 2013 c-myc but not Hif-1alpha-dependent downregulation of VEGF influences the proliferation and differentiation of HL-60 cells induced by ATRA. Tretinoin 133-137 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 23588859-10 2013 In conclusion, our data demonstrate that VEGF plays an important role in the differentiation and proliferation of HL-60 cells; c-myc-dependent downregulation of VEGF induced by ATRA contributes to the differentiation of HL-60 cells. Tretinoin 177-181 MYC proto-oncogene, bHLH transcription factor Homo sapiens 127-132 22407764-5 2012 Further, our data suggest an antagonistic functional connection between BRG1 and MYC, whereby, refractoriness to RA and GC by BRG1 inactivation involves deregulation of MYC activity. Tretinoin 113-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 81-84 22341854-4 2012 We have shown here that the tumour suppressor TIS21 negatively regulated c-Myc expression during all-trans-retinoic acid (ATRA)-induced differentiation that accelerated differentiation and reduced proliferation of acute promyelocytic leukaemia (APL) HL-60 cells. Tretinoin 100-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 73-78 22341854-4 2012 We have shown here that the tumour suppressor TIS21 negatively regulated c-Myc expression during all-trans-retinoic acid (ATRA)-induced differentiation that accelerated differentiation and reduced proliferation of acute promyelocytic leukaemia (APL) HL-60 cells. Tretinoin 122-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 73-78 23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 43-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 222-227 23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 58-62 MYC proto-oncogene, bHLH transcription factor Homo sapiens 222-227 22407764-5 2012 Further, our data suggest an antagonistic functional connection between BRG1 and MYC, whereby, refractoriness to RA and GC by BRG1 inactivation involves deregulation of MYC activity. Tretinoin 113-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 169-172 20538039-1 2010 Our previous studies demonstrated that retinoic acid (RA)-induced reduction of both, the key glycolytic enzyme ENO1 and proliferation-promoting c-Myc, resulted in decreased vitality and invasiveness of the follicular thyroid carcinoma cell lines FTC-133 and FTC-238. Tretinoin 39-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149 22020439-10 2011 Phospho-MYC synergizes with retinoic acid to eliminate circulating leukaemic cells and to decrease the level of tumour invasion. Tretinoin 28-41 MYC proto-oncogene, bHLH transcription factor Homo sapiens 8-11 20538039-1 2010 Our previous studies demonstrated that retinoic acid (RA)-induced reduction of both, the key glycolytic enzyme ENO1 and proliferation-promoting c-Myc, resulted in decreased vitality and invasiveness of the follicular thyroid carcinoma cell lines FTC-133 and FTC-238. Tretinoin 54-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149 20723292-7 2010 The c-myc expression of HL-60 cells in ATRA + hucMSC group was lower than that in ATRA group (p < 0.05). Tretinoin 39-43 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9 20723292-7 2010 The c-myc expression of HL-60 cells in ATRA + hucMSC group was lower than that in ATRA group (p < 0.05). Tretinoin 82-86 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9 19550295-14 2010 CONCLUSIONS: Myc-N expression is reduced with cytotoxic agents and retinoic acid in neuroblastoma although Myc-N amplification remains the same. Tretinoin 67-80 MYC proto-oncogene, bHLH transcription factor Homo sapiens 13-16 19507250-5 2009 Notably, RAD001 (10 nM) significantly augmented ATRA-induced expression of CCAAT/enhancer-binding protein epsilon (C/EBPepsilon) and p27(kip1) and downregulated levels of c-Myc in these cells. Tretinoin 48-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 171-176 19550295-15 2010 Retinoic acid combined with vincristine is the most effective combination to reduce Myc-N expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 84-87 19060179-9 2009 Both, RA-mediated and specific knock-down of ENO1/MBP-1 resulted in the reduction of MYC oncoprotein, and simultaneously decreased proliferation rates of FTC-133 and FTC-238 cell lines. Tretinoin 6-8 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-88 19324018-0 2009 All-trans retinoic acid induces Thrombospondin-1 expression in acute promyelocytic leukemia cells though down-regulation of its transcription repressor, c-MYC oncoprotein. Tretinoin 10-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 153-158 19324018-2 2009 The aim of the present study was to evaluate the role of c-MYC, a key transcription factor that contributes to the genesis of many human tumors, in TSP-1 induction by ATRA in acute promyelocytic leukemia (APL). Tretinoin 167-171 MYC proto-oncogene, bHLH transcription factor Homo sapiens 57-62 19324018-3 2009 ATRA treatment markedly increased TSP-1 level and inhibited c-MYC expression in NB4 APL leukemic cells compared with controls. Tretinoin 0-4 MYC proto-oncogene, bHLH transcription factor Homo sapiens 60-65 19324018-5 2009 c-MYC recruitment to TSP-1 promoter was dramatically decreased in NB4 cells following ATRA treatment. Tretinoin 86-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 19324018-7 2009 Moreover, transient over-expression of c-MYC totally abolished TSP-1 induction by ATRA in NB4 cells. Tretinoin 82-86 MYC proto-oncogene, bHLH transcription factor Homo sapiens 39-44 19324018-8 2009 Collectively, our results indicate that ATRA induces TSP-1 expression in APL cells though down-regulation of its transcription repressor, c-MYC oncoprotein. Tretinoin 40-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 138-143 19060179-10 2009 In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies. Tretinoin 16-18 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-77 19060179-10 2009 In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies. Tretinoin 173-175 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-77 18642056-5 2008 C-myc was down regulated by treatment with ATRA, alpha-TS and their combination to 22%, 48.5%, and 52%, respectively. Tretinoin 43-47 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 19115248-2 2009 The combined action of tamoxifen/all-trans retinoic acid was advantageous in MCF-7 cells, reducing cell proliferation, Bcl-2 and c-Myc protein levels and increasing E-Cadherin protein levels and Gap junctional Intercellular Communication. Tretinoin 43-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 129-134 19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 MYC proto-oncogene, bHLH transcription factor Homo sapiens 146-151 17706770-0 2008 Role of Myc in differentiation and apoptosis in HL60 cells after exposure to arsenic trioxide or all-trans retinoic acid. Tretinoin 97-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 8-11 18026954-4 2008 NB4 and R4 cells express BP1, bcl-2, and c-myc; the expression of all three genes was repressed after ATRA treatment of NB4 cells but not R4 cells. Tretinoin 102-106 MYC proto-oncogene, bHLH transcription factor Homo sapiens 41-46 17706770-4 2008 Characterization of expression and activity of c-Myc and its target genes hTERT (human telomerase reverse transcriptase) and CAD (carbamoyltransferase-dihydroorotase) revealed marked down-regulation in response to ATRA, but not As2O3. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 17453147-12 2007 In conclusion, we have provided evidence for the first time that RA may induce cell cycle arrest in vitro in DAOY MB cells via inhibition of CyclinD1 or C-myc. Tretinoin 65-67 MYC proto-oncogene, bHLH transcription factor Homo sapiens 153-158 16800923-9 2006 There was a substantial decrease in c-myc mRNA levels when 100 microg/ml bestatin was added to 10 nmol/L ATRA (P < 0.05). Tretinoin 105-109 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-41 17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 10-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-175 17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 25-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-175 17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 125-127 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-175 16800923-10 2006 Various concentrations (50, 75, 100 microg/ml) of bestatin combined with 10 nmol/L ATRA down-regulated the expression of c-Myc protein, which was negatively correlated with the NBT reduction activity of NB4 cells induced by 10 nmol/L ATRA alone or plus bestatin at various concentrations (r = -0.940, P = 0.017). Tretinoin 83-87 MYC proto-oncogene, bHLH transcription factor Homo sapiens 121-126 16800923-10 2006 Various concentrations (50, 75, 100 microg/ml) of bestatin combined with 10 nmol/L ATRA down-regulated the expression of c-Myc protein, which was negatively correlated with the NBT reduction activity of NB4 cells induced by 10 nmol/L ATRA alone or plus bestatin at various concentrations (r = -0.940, P = 0.017). Tretinoin 234-238 MYC proto-oncogene, bHLH transcription factor Homo sapiens 121-126 16800923-12 2006 It is concluded that an aminopeptidase inhibitor bestatin can potentiate ATRA-inducing differentiation of NB4 cells, possibly by down-regulating c-myc expression in synergy with ATRA. Tretinoin 73-77 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150 11877298-0 2002 Retinoic acid-induced cell cycle arrest of human myeloid cell lines is associated with sequential down-regulation of c-Myc and cyclin E and posttranscriptional up-regulation of p27(Kip1). Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 117-122 15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 336-341 16054129-5 2005 It was found that the kinetics of c-Myc correlates most closely with the telomerase activity suggesting in agreement with previous studies that this protein is a major intermediate of the RA-induced downregulation of telomerase activity. Tretinoin 188-190 MYC proto-oncogene, bHLH transcription factor Homo sapiens 34-39 15589822-0 2004 c-Myc-mediated expression of nucleophosmin/B23 decreases during retinoic acid-induced differentiation of human leukemia HL-60 cells. Tretinoin 64-77 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 15589822-1 2004 The retinoic acid-induced differentiation of human leukemia HL-60 cells towards mature granulocytic cells was accompanied by the decline in the protein levels of c-myc, nucleophosmin/B23 and its promoter activity. Tretinoin 4-17 MYC proto-oncogene, bHLH transcription factor Homo sapiens 162-167 12955881-6 2003 Retinoic acid also modulates c-myc and Bcl-2 expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 29-34 12637327-0 2003 Ser727/Tyr701-phosphorylated Stat1 is required for the regulation of c-Myc, cyclins, and p27Kip1 associated with ATRA-induced G0/G1 arrest of U-937 cells. Tretinoin 113-117 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-74 12637327-7 2003 Our results show that Ser727/Tyr701-phosphorylated Stat1 plays a key role as a prerequisite for the ATRA-induced down-regulation of c-Myc; cyclins A, B, D2, D3, and E; and the simultaneous up-regulation of p27Kip1, associated with arrest in the G0/G1 phase of the cell cycle. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 132-137 12513735-4 2002 It is concluded that the telomerase activity is related to decrease expression of hTERT, c-myc and bcl-2 mRNA during HL-60 cell differentiation induced by ATRA. Tretinoin 155-159 MYC proto-oncogene, bHLH transcription factor Homo sapiens 89-94 11877298-3 2002 In this study, we show that the onset of ATRA-induced G(0)/G(1) arrest of human monoblastic U-937 cells is linked to a sharp down-regulation of c-Myc and cyclin E levels and an increase in p21(WAF1/CIP1) expression. Tretinoin 41-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149 11877298-5 2002 The importance of an early decrease in Myc expression for these events was demonstrated by the failure of a U-937 subline with constitutive exogenous expression of v-Myc to cell cycle arrest and regulate cyclin E and p27(Kip1) in response to ATRA. Tretinoin 242-246 MYC proto-oncogene, bHLH transcription factor Homo sapiens 39-42 11877298-8 2002 These results thus identify a decrease in c-Myc and cyclin E levels and a posttranscriptional up-regulation of p27(Kip1) as important early changes, and position them in the complex chain of events regulating ATRA-induced cell cycle arrest of myeloid cells. Tretinoin 209-213 MYC proto-oncogene, bHLH transcription factor Homo sapiens 42-47 11776079-0 2000 c-myc gene inactivation during induction of nasopharyngeal carcinoma cells with retinoic acid. Tretinoin 80-93 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 11776079-9 2000 c-myc was down-regulated at 48 h of RA treatment. Tretinoin 36-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 11776079-15 2000 CONCLUSION: RA can induce differentiation in a nasopharyngeal carcinoma cell line at high concentration of RA; HNE1 shows some similar patterns of DNase I hypersensitive sites with the common one in other types of cells expressing c-myc. Tretinoin 12-14 MYC proto-oncogene, bHLH transcription factor Homo sapiens 231-236 8018561-5 1994 This fragment included the E2F binding site in the c-myc P2 promoter region, and a difference of shifted bands between RA-treated and untreated HL60 cells was due to complex formation of E2F and retinoblastoma protein. Tretinoin 119-121 MYC proto-oncogene, bHLH transcription factor Homo sapiens 51-56 10689181-7 2000 Increased centre of nucleus-to-gene and gene-to-gene distances of c-myc genes, centromeric region of chromosome 8 and chromosome 8 domains were found early after the induction of granulocytic differentiation by dimethyl sulfoxide (DMSO) or retinoic acid (RA); the size of the chromosome 8 domains was rapidly reduced. Tretinoin 240-253 MYC proto-oncogene, bHLH transcription factor Homo sapiens 66-71 10689181-7 2000 Increased centre of nucleus-to-gene and gene-to-gene distances of c-myc genes, centromeric region of chromosome 8 and chromosome 8 domains were found early after the induction of granulocytic differentiation by dimethyl sulfoxide (DMSO) or retinoic acid (RA); the size of the chromosome 8 domains was rapidly reduced. Tretinoin 255-257 MYC proto-oncogene, bHLH transcription factor Homo sapiens 66-71 10642512-1 2000 Retinoic acid-mediated differentiation of HL60 cells is associated with an alteration of chromatin structure that maps to protein-binding sequences within intron I of the c-myc gene and with down-regulation of c-myc expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 171-176 10642512-1 2000 Retinoic acid-mediated differentiation of HL60 cells is associated with an alteration of chromatin structure that maps to protein-binding sequences within intron I of the c-myc gene and with down-regulation of c-myc expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 210-215 10642512-6 2000 We also show that the time course of MIBP1 and RFX1 induction is inversely correlated with the down-regulation of c-myc levels during the treatment of HL60 cells with retinoic acid. Tretinoin 167-180 MYC proto-oncogene, bHLH transcription factor Homo sapiens 114-119 12548778-4 1999 In RA-sensitive cell lines, ATRA-induced G0/G1 arrest is associated with down regulaton of c-myc and hyperphosphorylated Rb expression, and up regulation of p21WAF1/CIP1 and p53 expression. Tretinoin 28-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 91-96 9804832-0 1998 c-Myc is a major mediator of the synergistic growth inhibitory effects of retinoic acid and interferon in breast cancer cells. Tretinoin 74-87 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5 9804832-7 1998 When c-Myc was overexpressed ectopically via a c-Myc expression vector, MCF-7 cells became resistant to growth inhibition by all-trans-retinoic acid plus interferon-alpha. Tretinoin 125-148 MYC proto-oncogene, bHLH transcription factor Homo sapiens 5-10 9804832-7 1998 When c-Myc was overexpressed ectopically via a c-Myc expression vector, MCF-7 cells became resistant to growth inhibition by all-trans-retinoic acid plus interferon-alpha. Tretinoin 125-148 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52 9804832-8 1998 These experiments define the following pathway as a major pathway in the synergistic growth inhibition of MCF-7 cells by all-trans-retinoic acid plus interferon-alpha: all-trans-retinoic acid + interferon-alpha --> upward arrow double-stranded RNA-dependent protein kinase --> downward arrow c-Myc --> cell growth inhibition. Tretinoin 131-144 MYC proto-oncogene, bHLH transcription factor Homo sapiens 298-303 9494568-0 1997 Effects of tamoxifen and retinoic acid on cell growth and c-myc gene expression in human breast and cervical cancer cells. Tretinoin 25-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 58-63 10743138-2 1997 The results indicated that after treated with ST and RA, the cells became well-differentiated, the cell growth was suppressed, contact suppress was partially recovered, colony forming was decreased, protooncogenes (C-myc bcl-2) protein was decreased, tumor suppressor gene (p53) protein was increased. Tretinoin 53-55 MYC proto-oncogene, bHLH transcription factor Homo sapiens 215-220 10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 151-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 64-69 10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 151-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 213-218 10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 166-168 MYC proto-oncogene, bHLH transcription factor Homo sapiens 64-69 10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 166-168 MYC proto-oncogene, bHLH transcription factor Homo sapiens 213-218 8934535-2 1996 We have previously reported that all-trans-retinoic acid (RA) inhibits the growth of NCI-H82 SCLC cells in association with increased neuroendocrine differentiation, increased L-myc gene expression and decreased c-myc gene expression. Tretinoin 33-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 212-217 8934535-2 1996 We have previously reported that all-trans-retinoic acid (RA) inhibits the growth of NCI-H82 SCLC cells in association with increased neuroendocrine differentiation, increased L-myc gene expression and decreased c-myc gene expression. Tretinoin 58-60 MYC proto-oncogene, bHLH transcription factor Homo sapiens 212-217 8519445-4 1995 Retinoic acid decreased N-myc and c-myc and induced neurite outgrowth (a differentiation marker). Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 34-39 10984118-0 2000 A combination treatment of c-myc antisense DNA with all-trans-retinoic acid inhibits cell proliferation by downregulating c-myc expression in small cell lung cancer. Tretinoin 52-75 MYC proto-oncogene, bHLH transcription factor Homo sapiens 27-32 10984118-0 2000 A combination treatment of c-myc antisense DNA with all-trans-retinoic acid inhibits cell proliferation by downregulating c-myc expression in small cell lung cancer. Tretinoin 52-75 MYC proto-oncogene, bHLH transcription factor Homo sapiens 122-127 10984118-2 2000 In this study, we investigated whether c-myc antisense oligodeoxynucleoside phosphorothioate (OPT) covering the translational initiation site of c-myc mRNA used in combination with all-trans-retinoic acid (RA) would be more effective than either agent alone in inhibiting the growth of an SCLC cell line, NCI-H82, overexpressing c-myc with amplification of this gene, and whether this combination could be an experimental therapeutic tool against SCLC. Tretinoin 206-208 MYC proto-oncogene, bHLH transcription factor Homo sapiens 39-44 10984118-2 2000 In this study, we investigated whether c-myc antisense oligodeoxynucleoside phosphorothioate (OPT) covering the translational initiation site of c-myc mRNA used in combination with all-trans-retinoic acid (RA) would be more effective than either agent alone in inhibiting the growth of an SCLC cell line, NCI-H82, overexpressing c-myc with amplification of this gene, and whether this combination could be an experimental therapeutic tool against SCLC. Tretinoin 206-208 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150 10984118-2 2000 In this study, we investigated whether c-myc antisense oligodeoxynucleoside phosphorothioate (OPT) covering the translational initiation site of c-myc mRNA used in combination with all-trans-retinoic acid (RA) would be more effective than either agent alone in inhibiting the growth of an SCLC cell line, NCI-H82, overexpressing c-myc with amplification of this gene, and whether this combination could be an experimental therapeutic tool against SCLC. Tretinoin 206-208 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150 10896783-4 2000 Furthermore, RA-induced growth arrest of CH27 cells was also associated with increased retinoic acid receptor beta (RARbeta) and reduced c-Myc expression. Tretinoin 13-15 MYC proto-oncogene, bHLH transcription factor Homo sapiens 137-142 10760826-0 2000 Retinoic acid induces persistent, RARalpha-mediated anti-proliferative responses in Epstein-Barr virus-immortalized b lymphoblasts carrying an activated C-MYC oncogene but not in Burkitt"s lymphoma cell lines. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 153-158 10074929-0 1999 Retinoic acid-mediated growth inhibition of small cell lung cancer cells is associated with reduced myc and increased p27Kip1 expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 100-103 9740074-2 1998 Because preclinical data showed that all-trans-retinoic acid (RA) inhibited SCLC growth, altered myc expression, and blocked transition to a treatment-resistant phenotype, a Phase II trial was designed to determine the effects of the combination of RA, cisplatin, and etoposide in patients with SCLC. Tretinoin 37-60 MYC proto-oncogene, bHLH transcription factor Homo sapiens 97-100 9740074-2 1998 Because preclinical data showed that all-trans-retinoic acid (RA) inhibited SCLC growth, altered myc expression, and blocked transition to a treatment-resistant phenotype, a Phase II trial was designed to determine the effects of the combination of RA, cisplatin, and etoposide in patients with SCLC. Tretinoin 62-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 97-100 9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 33-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 65-70 9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 224-228 MYC proto-oncogene, bHLH transcription factor Homo sapiens 65-70 9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 39-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 65-70 9290118-4 1997 An increase in c-myc expression after supplementation was observed in 6 of 12 subjects, but 5 of these 6 subjects had decreased total serum retinoic acid concentration and 4 had decreased ATRA concentration. Tretinoin 140-153 MYC proto-oncogene, bHLH transcription factor Homo sapiens 15-20 9290118-4 1997 An increase in c-myc expression after supplementation was observed in 6 of 12 subjects, but 5 of these 6 subjects had decreased total serum retinoic acid concentration and 4 had decreased ATRA concentration. Tretinoin 188-192 MYC proto-oncogene, bHLH transcription factor Homo sapiens 15-20 9290118-6 1997 Conversely, c-myc expression was increased in only two of five paired samples from subjects whose total serum retinoic acid concentration increased during the 90-day supplementation period. Tretinoin 110-123 MYC proto-oncogene, bHLH transcription factor Homo sapiens 12-17 7656409-0 1995 Reversal of alcohol"s effects on neurite extension and on neuronal GAP43/B50, N-myc, and c-myc protein levels by retinoic acid. Tretinoin 113-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 89-94 7656409-6 1995 These retinoic acid-induced increases in GAP43/B50 and neurite outgrowth, and decreases in N-myc and c-myc, were reversed dose-dependently by alcohol (0-0.5%). Tretinoin 6-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 101-106 7656409-7 1995 Conversely, the adverse effects of 0.25% alcohol on neurite extension, GAP43/B50, N-myc, and c-myc were prevented by 15 and 45 nM retinoic acid. Tretinoin 130-143 MYC proto-oncogene, bHLH transcription factor Homo sapiens 93-98 7656409-8 1995 These results suggest that inhibition of neuronal differentiation by alcohol and prevention of such effects by retinoic acid are related to changes in GAP43/B50, N-myc and c-myc. Tretinoin 111-124 MYC proto-oncogene, bHLH transcription factor Homo sapiens 172-177 7768638-0 1995 Retinoic acid induced death of ovarian carcinoma cells correlates with c-myc stimulation. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 71-76 7768638-3 1995 Exposure of N.I cells to increasing concentrations of ATRA was accompanied by a considerable up-regulation of c-myc transcript levels that correlated with the rate of cell killing, which itself was an active process as judged by sustained transcriptional expression. Tretinoin 54-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 110-115 7768638-6 1995 The accompanying c-myc up-regulation seems to be mediated by retinoic-acid-receptor-independent pathways involving membrane-associated phospholipases instead, because manoalide partly suppressed c-myc induction by ATRA but left constitutive c-myc expression unaffected. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 17-22 7768638-6 1995 The accompanying c-myc up-regulation seems to be mediated by retinoic-acid-receptor-independent pathways involving membrane-associated phospholipases instead, because manoalide partly suppressed c-myc induction by ATRA but left constitutive c-myc expression unaffected. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 195-200 7768638-6 1995 The accompanying c-myc up-regulation seems to be mediated by retinoic-acid-receptor-independent pathways involving membrane-associated phospholipases instead, because manoalide partly suppressed c-myc induction by ATRA but left constitutive c-myc expression unaffected. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 195-200 8018561-6 1994 The present results suggest that E2F plays an important role in the process of cell differentiation by RA and that a change of the E2F binding pattern induced by RA contributes to the suppression of c-myc gene expression preceding granulocytic differentiation. Tretinoin 162-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 199-204 8239509-1 1993 Retinoic acid (RA) modulation of c-myc and max gene expression was investigated in human breast carcinoma (HBC) cell lines. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38 8123593-0 1994 All-trans-retinoic acid alters myc gene expression and inhibits in vitro progression in small cell lung cancer. Tretinoin 0-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 31-34 8123593-4 1994 We now report that treatment of NCI-H82 cells with 1 microM all-trans-retinoic acid resulted in decreased cellular growth, decreased c-myc mRNA levels, and increased L-myc mRNA levels. Tretinoin 60-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 133-138 8123593-7 1994 These data show that all-trans-retinoic acid, a clinically relevant compound, inhibits small cell lung cancer progression in our in vitro model and alters the expression of the c-myc and L-myc oncogenes. Tretinoin 21-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 177-182 8274449-4 1993 Of interest, 5 SCLC lines with high levels of myc gene family expression related to c-, N-, or L-myc gene amplification exhibited growth inhibition (28-87%), whereas 2 non-SCLC lines actually showed growth stimulation after treatment with 1 microM RA. Tretinoin 248-250 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-49 8239509-1 1993 Retinoic acid (RA) modulation of c-myc and max gene expression was investigated in human breast carcinoma (HBC) cell lines. Tretinoin 15-17 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38 8239509-3 1993 RA-mediated increase in c-myc mRNA levels were noticed as early as 30 min. Tretinoin 0-2 MYC proto-oncogene, bHLH transcription factor Homo sapiens 24-29 8239509-5 1993 We thus report for the first time that RA, during its growth inhibitory effects on MCF-7 HBC cells, positively regulates the gene expression of c-myc and max. Tretinoin 39-41 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149 8396695-4 1993 In addition, we observed that RA and 16-23-D3 interact additively with respect to the reduction of c-myc mRNA expression. Tretinoin 30-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 99-104 1429370-6 1992 Amongst the agents considered, retinoic acid was the only one that caused a significant parallel reduction in RB and c-myc expression in the HL-60 human promyelocytic leukemia cells tested. Tretinoin 31-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 117-122 8490200-0 1993 Inhibition of c-myc in breast and ovarian carcinoma cells by 1,25-dihydroxyvitamin D3, retinoic acid and dexamethasone. Tretinoin 87-100 MYC proto-oncogene, bHLH transcription factor Homo sapiens 14-19 8490200-2 1993 The downregulation of the c-myc protooncogene by 1,25-dihydroxyvitamin D3 (calcitriol), retinoic acid (RA) and dexamethasone (Dex) is closely associated with growth inhibition in leukemic cells. Tretinoin 88-101 MYC proto-oncogene, bHLH transcription factor Homo sapiens 26-31 1478951-6 1992 Densitometer evaluation of electrophoresed proteins revealed a 50% DMSO- and a 25% RA-induced myc reduction. Tretinoin 83-85 MYC proto-oncogene, bHLH transcription factor Homo sapiens 94-97 1478951-7 1992 Apart from growth reduction, which was seen for both inducers, inhibition of myc gene expression was the only response of HOC-7 cells to RA-treatment. Tretinoin 137-139 MYC proto-oncogene, bHLH transcription factor Homo sapiens 77-80 8518028-4 1993 Recombinant human granulocyte-macrophage colony-stimulating factor (RhGM-CSF) can increase and retinoic acid/alpha-interferon can decrease c-myc expression in myeloid cells in vivo. Tretinoin 95-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 139-144 1637683-8 1992 All four agents inhibited myc oncoprotein expression reversibly (1% DMSO greater than 0.5% DMF greater than 10 microM RA greater than 10 ng ml-1 TGF-beta 1) and in time-dependent manner. Tretinoin 118-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 26-29