PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24637737-2 2014 In the present study, we designed antisense oligonucleotides (ASOs) against MDR1, MDR-associated protein (MRP)1, MRP2, and/or BCL-2/BCL-xL to reverse MDR transporters and induce apoptosis, respectively. Oligonucleotides 44-60 BCL2 like 1 Homo sapiens 132-138 29246296-0 2017 Antisense Oligonucleotides Targeting Y-Box Binding Protein-1 Inhibit Tumor Angiogenesis by Downregulating Bcl-xL-VEGFR2/-Tie Axes. Oligonucleotides 10-26 BCL2 like 1 Homo sapiens 106-112 26718027-0 2016 Pro-apoptotic effects of splice-switching oligonucleotides targeting Bcl-x pre-mRNA in human glioma cell lines. Oligonucleotides 42-58 BCL2 like 1 Homo sapiens 69-74 27579319-8 2016 Redirection of Bcl-x splicing by an antisense oligonucleotide from the antiapoptotic isoform to the proapoptotic isoform induced death of HSCs without other apoptosis stimuli. Oligonucleotides 46-61 BCL2 like 1 Homo sapiens 15-20 17224645-3 2007 In addition, we have shown that down regulation of BCL-X(L) using a BCL-X(L) antisense oligonucleotide engenders mesothelioma apoptotic cell death in vitro and in vivo. Oligonucleotides 87-102 BCL2 like 1 Homo sapiens 51-59 23480956-4 2013 Antisense oligonucleotide (ASON) Bcl-xl could be encapsulated into this hybrid nanosystem with extremely high loading efficiency by a nanoemulsion technique. Oligonucleotides 10-25 BCL2 like 1 Homo sapiens 33-39 23353574-8 2013 The use of endogenous inhibitors of bcl-xL and other anti-apoptotic genes such as hsa-miR-15a-3p may provide improved options for apoptosis-modulating therapies in cancer treatment compared with the use of artificial antisense oligonucleotides. Oligonucleotides 227-243 BCL2 like 1 Homo sapiens 36-42 17697540-13 2007 The expression of STAT3, p-STAT3, and Bcl-x(L) were down-regulated after transfection of antisense oligonucleotide. Oligonucleotides 99-114 BCL2 like 1 Homo sapiens 38-46 17224645-3 2007 In addition, we have shown that down regulation of BCL-X(L) using a BCL-X(L) antisense oligonucleotide engenders mesothelioma apoptotic cell death in vitro and in vivo. Oligonucleotides 87-102 BCL2 like 1 Homo sapiens 68-76 16412215-4 2006 RESULTS: We show that an oligonucleotide with a 5" tail containing the human beta-globin branch site sequence inhibits the use of the 5" splice site of Bcl-xL, albeit less efficiently than a tail containing binding sites for the hnRNP A1/A2 proteins. Oligonucleotides 25-40 BCL2 like 1 Homo sapiens 152-158 18029612-0 2007 Inhibition of bcl-xL expression by antisense oligonucleotides containing various bridged nucleic acids (BNAs). Oligonucleotides 45-61 BCL2 like 1 Homo sapiens 14-20 17172421-4 2006 As anticancer agent, we encapsulated the previously described antisense oligonucleotide 4625 specific for both bcl-2 and bcl-xL. Oligonucleotides 72-87 BCL2 like 1 Homo sapiens 121-127 16686729-0 2006 Induction of apoptosis and enhancement of chemosensitivity in human prostate cancer LNCaP cells using bispecific antisense oligonucleotide targeting Bcl-2 and Bcl-xL genes. Oligonucleotides 123-138 BCL2 like 1 Homo sapiens 159-165 16686729-1 2006 OBJECTIVE: To determine whether a specifically designed bispecific (Bcl-2/Bcl-xL) antisense oligonucleotide (ASO) induces apoptosis and enhances chemosensitivity in human prostate cancer LNCaP cells, as Bcl-2 and Bcl-xL are both anti-apoptotic genes associated with treatment resistance and tumour progression in many malignancies, including prostate cancer. Oligonucleotides 92-107 BCL2 like 1 Homo sapiens 74-80 16374552-6 2006 Treatment with a subtoxic concentration of a bispecific bcl-2/bcl xL antisense oligonucleotide cooperated with okadaic acid to down-regulate bcl-2 and sensitize cyclin D1-overexpressing cells to okadaic acid. Oligonucleotides 79-94 BCL2 like 1 Homo sapiens 62-68 16275990-2 2005 The objective of this study was to determine whether a novel bispecific antisense oligonucleotide targeting both Bcl-2 and Bcl-xL induces apoptosis and enhances chemosensitivity in androgen-independent PC3 prostate cancer cells. Oligonucleotides 82-97 BCL2 like 1 Homo sapiens 123-129 17150931-3 2006 Our data revealed that 2",4"-BNA antisense oligonucleotides remarkably inhibited the expression of bcl-xL in HepG2 cells compared to the natural DNA antisense oligonucleotide. Oligonucleotides 43-59 BCL2 like 1 Homo sapiens 99-105 17150931-3 2006 Our data revealed that 2",4"-BNA antisense oligonucleotides remarkably inhibited the expression of bcl-xL in HepG2 cells compared to the natural DNA antisense oligonucleotide. Oligonucleotides 43-58 BCL2 like 1 Homo sapiens 99-105 16299354-3 2005 Here, we show that a short antisense chimeric peptide nucleic acid (PNA) oligonucleotide conjugated to a polypeptide containing eight Ser-Arg repeats (SR)(8) can modulate splicing of bcl-x both in vitro and in vivo and induces apoptosis in HeLa cells. Oligonucleotides 73-88 BCL2 like 1 Homo sapiens 183-188 16275990-3 2005 An antisense oligonucleotide with complete sequence identity to Bcl-2 and three-base mismatches to Bcl-xL selected from five antisense oligonucleotides targeting various regions with high homology between Bcl-2 and Bcl-xL was found to be the most potent inhibitor of both Bcl-2 and Bcl-xL expression in PC3 cells. Oligonucleotides 13-28 BCL2 like 1 Homo sapiens 99-105 16275990-3 2005 An antisense oligonucleotide with complete sequence identity to Bcl-2 and three-base mismatches to Bcl-xL selected from five antisense oligonucleotides targeting various regions with high homology between Bcl-2 and Bcl-xL was found to be the most potent inhibitor of both Bcl-2 and Bcl-xL expression in PC3 cells. Oligonucleotides 13-28 BCL2 like 1 Homo sapiens 215-221 16275990-3 2005 An antisense oligonucleotide with complete sequence identity to Bcl-2 and three-base mismatches to Bcl-xL selected from five antisense oligonucleotides targeting various regions with high homology between Bcl-2 and Bcl-xL was found to be the most potent inhibitor of both Bcl-2 and Bcl-xL expression in PC3 cells. Oligonucleotides 13-28 BCL2 like 1 Homo sapiens 215-221 16275990-3 2005 An antisense oligonucleotide with complete sequence identity to Bcl-2 and three-base mismatches to Bcl-xL selected from five antisense oligonucleotides targeting various regions with high homology between Bcl-2 and Bcl-xL was found to be the most potent inhibitor of both Bcl-2 and Bcl-xL expression in PC3 cells. Oligonucleotides 135-151 BCL2 like 1 Homo sapiens 99-105 16275990-4 2005 This selected Bcl-2/Bcl-xL bispecific antisense oligonucleotide reduced mRNA and protein levels in a dose-dependent manner, reducing Bcl-2 and Bcl-xL protein levels to 12% and 19%, respectively. Oligonucleotides 48-63 BCL2 like 1 Homo sapiens 20-26 16275990-4 2005 This selected Bcl-2/Bcl-xL bispecific antisense oligonucleotide reduced mRNA and protein levels in a dose-dependent manner, reducing Bcl-2 and Bcl-xL protein levels to 12% and 19%, respectively. Oligonucleotides 48-63 BCL2 like 1 Homo sapiens 143-149 16275990-8 2005 This Bcl-2/Bcl-xL bispecific antisense oligonucleotide also enhanced paclitaxel chemosensitivity in PC3 cells, reducing the IC50 of paclitaxel by >90%. Oligonucleotides 39-54 BCL2 like 1 Homo sapiens 11-17 15505422-6 2004 Bcl-2/bclxL-specific antisense oligonucleotides restored the sensitivity of SK-OV-3 cells to apoptosis induction by rapamycin and RAD001. Oligonucleotides 31-47 BCL2 like 1 Homo sapiens 6-11 16085054-7 2005 The inhibition of PXR expression by antisense oligonucleotide abolished PXR activators Bcl-xL induction. Oligonucleotides 46-61 BCL2 like 1 Homo sapiens 87-93 15917659-6 2005 Treatment of HeP2 and Cal27 cells with 400 nM antisense oligonucleotides against Bcl-2, Bcl-X(L) and Survivin for 48 hrs decreased their expression both at the mRNA as well as at the protein level, resulting in the induction of apoptosis. Oligonucleotides 56-72 BCL2 like 1 Homo sapiens 88-96 15820062-2 2005 This study was to explore regulatory effect of STAT5 decoy oligonucleotides (ODNs) on trans-activation of its downstream target bcl-x gene in K562 cells. Oligonucleotides 59-75 BCL2 like 1 Homo sapiens 128-133 15570009-0 2004 Trastuzumab down-regulates Bcl-2 expression and potentiates apoptosis induction by Bcl-2/Bcl-XL bispecific antisense oligonucleotides in HER-2 gene--amplified breast cancer cells. Oligonucleotides 117-133 BCL2 like 1 Homo sapiens 89-95 15820062-0 2005 [Regulatory effect of STAT5 decoy oligonucleotides on trans-activation of bcl-x gene promoter in K562 cells]. Oligonucleotides 34-50 BCL2 like 1 Homo sapiens 74-79 15375570-4 2004 The knockdown was accomplished by second-generation chimeric antisense oligonucleotides: Bcl-2 and Bcl-xL levels were strongly and reproducibly reduced, as revealed by real-time RT-PCR and Western blot analyses. Oligonucleotides 71-87 BCL2 like 1 Homo sapiens 99-105 15379893-6 2004 Cyclic AMP responsive element decoy oligonucleotides markedly attenuated the UTP-induced increase in bcl-2 and bcl-xl mRNA levels. Oligonucleotides 36-52 BCL2 like 1 Homo sapiens 111-117 15625915-0 2004 A functionally improved locked nucleic acid antisense oligonucleotide inhibits Bcl-2 and Bcl-xL expression and facilitates tumor cell apoptosis. Oligonucleotides 54-69 BCL2 like 1 Homo sapiens 89-95 15159020-5 2004 Down-regulation of either PKCeta or Bcl-xL in combination with vincristine or paclitaxel resulted in a significant increase in caspase-3 activity compared to that in the control oligonucleotide treated cells. Oligonucleotides 178-193 BCL2 like 1 Homo sapiens 36-42 14676192-8 2004 Down-regulation of Bcl-X(L) by antisense oligonucleotides or the newly identified Bcl-X(L) inhibitor chelerythrine restores cellular sensitivity to injury and death. Oligonucleotides 41-57 BCL2 like 1 Homo sapiens 19-27 15332326-3 2004 Down-regulation of Bcl-xL and Bcl-2 with DNA antisense oligonucleotides promotes cell death in glioblastoma cells. Oligonucleotides 55-71 BCL2 like 1 Homo sapiens 19-25 14960579-7 2004 Whereas overexpression of Bcl-2 significantly attenuated IL-18-induced endothelial cell apoptosis, Bcl-2/Bcl-X(L) chimeric phosphorothioated 2"-MOE-modified antisense oligonucleotides potentiated the proapoptotic effects of IL-18. Oligonucleotides 167-183 BCL2 like 1 Homo sapiens 105-113 15141012-0 2004 Antisense oligonucleotides directed at the bcl-xl gene product augment chemotherapy response in mesothelioma. Oligonucleotides 10-26 BCL2 like 1 Homo sapiens 43-49 15141012-5 2004 We sought to determine whether antisense oligonucleotides directed at the bcl-xl gene product would augment response to a conventional chemotherapeutic agent in human mesothelioma cell lines. Oligonucleotides 41-57 BCL2 like 1 Homo sapiens 74-80 15141012-11 2004 Western blot demonstrated 15999 antisense oligonucleotides construct down-regulation of BCL-XL, but no further effect on expression of BCL-2 proteins with cisplatin. Oligonucleotides 42-58 BCL2 like 1 Homo sapiens 88-94 15141012-13 2004 CONCLUSIONS: Exposure of human MPM cells to bcl-xl antisense oligonucleotides sensitizes human mesothelioma cells to the conventional chemotherapeutic agent cisplatin. Oligonucleotides 61-77 BCL2 like 1 Homo sapiens 44-50 14985457-10 2004 A 2"-O-ribose methoxyethyl phosphorothioate antisense oligonucleotide reduced Bcl-xl protein expression by approximately 90% in HCT116 (Bcl-xl knockdown). Oligonucleotides 54-69 BCL2 like 1 Homo sapiens 78-84 14985457-10 2004 A 2"-O-ribose methoxyethyl phosphorothioate antisense oligonucleotide reduced Bcl-xl protein expression by approximately 90% in HCT116 (Bcl-xl knockdown). Oligonucleotides 54-69 BCL2 like 1 Homo sapiens 136-142 14522969-6 2003 In four different human cell lines, an interfering oligonucleotide carrying A1/A2 binding sites also shifted the alternative splicing of the Bcl-x pre-mRNA more efficiently than oligonucleotides acting through duplex formation only. Oligonucleotides 51-66 BCL2 like 1 Homo sapiens 141-146 15625915-1 2004 We previously reported the Bcl-2/Bcl-xL-bispecific activity of the 2"-O-(2-methoxy)ethyl (2"-MOE)-modified gapmer antisense oligonucleotide 4625. Oligonucleotides 124-139 BCL2 like 1 Homo sapiens 33-39 15625915-2 2004 This oligonucleotide has 100% complementarity to Bcl-2 and three mismatches to Bcl-xL. Oligonucleotides 5-20 BCL2 like 1 Homo sapiens 79-85 14520471-0 2003 Bcl-x(L) antisense oligonucleotides radiosensitise colon cancer cells. Oligonucleotides 19-35 BCL2 like 1 Homo sapiens 0-8 14627985-0 2003 Treatment of melanoma cells with a bcl-2/bcl-xL antisense oligonucleotide induces antiangiogenic activity. Oligonucleotides 58-73 BCL2 like 1 Homo sapiens 41-47 14627985-3 2003 In the present study, we demonstrated that the bcl-2/bcl-xL bispecific antisense oligonucleotide 4625 inhibits bcl-2 expression and angiogenesis in two bcl-2 overexpressing clones derived from the M14 human melanoma cell line. Oligonucleotides 81-96 BCL2 like 1 Homo sapiens 53-59 14520471-3 2003 Since approximately 60% of human colon cancers express Bcl-x(L), it was the aim of this study to explore the potential of Bcl-x(L) antisense oligonucleotides as a novel radiosensitisation strategy. Oligonucleotides 141-157 BCL2 like 1 Homo sapiens 122-130 14520471-5 2003 Bcl-x(L) antisense oligonucleotide specifically reduced the Bcl-x(L) protein level by almost 50% in Caco-2 cells. Oligonucleotides 19-34 BCL2 like 1 Homo sapiens 0-8 14520471-5 2003 Bcl-x(L) antisense oligonucleotide specifically reduced the Bcl-x(L) protein level by almost 50% in Caco-2 cells. Oligonucleotides 19-34 BCL2 like 1 Homo sapiens 60-68 14520471-8 2003 Specific reduction of Bcl-x(L) protein levels by antisense oligonucleotides qualifies as a promising therapeutic strategy for colon cancer that may help overcome resistance and improve clinical outcome in this malignancy. Oligonucleotides 59-75 BCL2 like 1 Homo sapiens 22-30 12452453-2 2002 Here we describe the use of the bcl-2/bcl-xL bispecific antisense oligonucleotide 4625 to sensitize breast carcinoma cells to anti-cancer drugs routinely used in breast cancer therapy. Oligonucleotides 66-81 BCL2 like 1 Homo sapiens 38-44 12800189-4 2003 Preferential downregulation of either Bcl-xL alone or of Bcl-xL and Bcl-2 simultaneously was achieved by treatment with antisense oligonucleotides 4259 and 4625, respectively, whereas the expression of other apoptosis-relevant genes remained unaffected. Oligonucleotides 130-146 BCL2 like 1 Homo sapiens 38-44 12800189-4 2003 Preferential downregulation of either Bcl-xL alone or of Bcl-xL and Bcl-2 simultaneously was achieved by treatment with antisense oligonucleotides 4259 and 4625, respectively, whereas the expression of other apoptosis-relevant genes remained unaffected. Oligonucleotides 130-146 BCL2 like 1 Homo sapiens 57-63 12855666-3 2003 RESULTS: A modified phosphorothioate antisense oligonucleotide (ISIS15999) reduced Bcl-xl protein expression by approximately 90%. Oligonucleotides 47-62 BCL2 like 1 Homo sapiens 83-89 12558990-3 2003 Down-regulation of both bcl-2 and bcl-xL expression in glioblastoma cell lines U87 and NS008 with bcl-2/bcl-xL bispecific antisense oligonucleotide resulted in spontaneous cell death. Oligonucleotides 132-147 BCL2 like 1 Homo sapiens 34-40 12558990-3 2003 Down-regulation of both bcl-2 and bcl-xL expression in glioblastoma cell lines U87 and NS008 with bcl-2/bcl-xL bispecific antisense oligonucleotide resulted in spontaneous cell death. Oligonucleotides 132-147 BCL2 like 1 Homo sapiens 104-110 12393593-6 2002 In contrast, B9 cells overexpressing FGFR3 were resistant to treatment with dexamethasone, a phenomenon successfully reversed using a Bcl-x(L) antisense oligonucleotide. Oligonucleotides 153-168 BCL2 like 1 Homo sapiens 134-142 12543166-9 2003 Moreover, the reduction of Bcl-X(L) by specific antisense oligonucleotide treatment enhanced the CH11-induced cell death of HSC-2. Oligonucleotides 58-73 BCL2 like 1 Homo sapiens 27-35 12381725-4 2002 It also suggests a specificity of the oligonucleotide effects since non-cancerous cells with low levels of Bcl-xL should resist the treatment. Oligonucleotides 38-53 BCL2 like 1 Homo sapiens 107-113 12570053-3 2002 Morpholino Bcl-xL antisense oligonucleotides (oligos) were employed to down-regulate Bcl-xL in CBDCA-resistant (MIT8, MIT16) as well as CBDCA-sensitive (MIT7) SCC cell lines. Oligonucleotides 28-44 BCL2 like 1 Homo sapiens 11-17 12570053-3 2002 Morpholino Bcl-xL antisense oligonucleotides (oligos) were employed to down-regulate Bcl-xL in CBDCA-resistant (MIT8, MIT16) as well as CBDCA-sensitive (MIT7) SCC cell lines. Oligonucleotides 28-44 BCL2 like 1 Homo sapiens 85-91 12570053-3 2002 Morpholino Bcl-xL antisense oligonucleotides (oligos) were employed to down-regulate Bcl-xL in CBDCA-resistant (MIT8, MIT16) as well as CBDCA-sensitive (MIT7) SCC cell lines. Oligonucleotides 46-52 BCL2 like 1 Homo sapiens 11-17 12570053-3 2002 Morpholino Bcl-xL antisense oligonucleotides (oligos) were employed to down-regulate Bcl-xL in CBDCA-resistant (MIT8, MIT16) as well as CBDCA-sensitive (MIT7) SCC cell lines. Oligonucleotides 46-52 BCL2 like 1 Homo sapiens 85-91 12218266-0 2002 Bcl-xL antisense oligonucleotides chemosensitize human glioblastoma cells. Oligonucleotides 17-33 BCL2 like 1 Homo sapiens 0-6 12218266-6 2002 CONCLUSION: Combination treatment using Bcl-xL antisense oligonucleotides and paclitaxel may qualify as a promising strategy to ultimately improve the clinical outcome of glioblastoma. Oligonucleotides 57-73 BCL2 like 1 Homo sapiens 40-46 12218266-2 2002 METHODS: Bcl-xL expression was specifically reduced in M059K glioblastoma cells with antisense oligonucleotides (ISIS 16009, ISIS 16967) as assessed by Western blotting. Oligonucleotides 95-111 BCL2 like 1 Homo sapiens 9-15 12218266-4 2002 RESULTS: Antisense oligonucleotide-mediated reduction of Bcl-xL levels led to enhanced cytotoxicity in M059K cells when compared to the use of a mismatch control oligonucleotide (p < 0.001). Oligonucleotides 19-34 BCL2 like 1 Homo sapiens 57-63 12218266-4 2002 RESULTS: Antisense oligonucleotide-mediated reduction of Bcl-xL levels led to enhanced cytotoxicity in M059K cells when compared to the use of a mismatch control oligonucleotide (p < 0.001). Oligonucleotides 162-177 BCL2 like 1 Homo sapiens 57-63 12070027-4 2002 Each antisense oligonucleotide (ASO; Bcl-2, Bcl-x(L), or Mcl-1 ASO) introduced into human myeloma cell lines by electroporation induced a marked reduction in the level of the corresponding protein. Oligonucleotides 15-30 BCL2 like 1 Homo sapiens 44-49 12063468-0 2002 Antisense therapy for malignant mesothelioma with oligonucleotides targeting the bcl-xl gene product. Oligonucleotides 50-66 BCL2 like 1 Homo sapiens 81-87 12031489-5 2002 Only oligonucleotide 4625 exhibited a potent bispecific antisense activity against bcl-2 and bcl-xL, which effectively reduced tumor cell viability. Oligonucleotides 5-20 BCL2 like 1 Homo sapiens 93-99 12031489-0 2002 Analysis of ribosyl-modified, mixed backbone analogs of a bcl-2/bcl-xL antisense oligonucleotide. Oligonucleotides 81-96 BCL2 like 1 Homo sapiens 64-70 12031489-2 2002 The ability of the 2"-O-(2-methoxyethylribose) (2"-MOE)-modified phosphorothioate gapmer oligonucleotide 4625, which matches the bcl-2 mRNA and has three base-mismatches to bcl-xL, to inhibit bcl-2 and bcl-xL expression and induce tumor cell apoptosis has been described. Oligonucleotides 89-104 BCL2 like 1 Homo sapiens 173-179 12031489-2 2002 The ability of the 2"-O-(2-methoxyethylribose) (2"-MOE)-modified phosphorothioate gapmer oligonucleotide 4625, which matches the bcl-2 mRNA and has three base-mismatches to bcl-xL, to inhibit bcl-2 and bcl-xL expression and induce tumor cell apoptosis has been described. Oligonucleotides 89-104 BCL2 like 1 Homo sapiens 202-208 12031489-4 2002 The ability of the various 4625 analogs, including the parental first-generation oligonucleotide 3005, to inhibit bcl-2 and bcl-xL expression, and diminish cell growth or induce tumor cell death was assessed in SW2 lung cancer cells using real-time PCR, Western blotting and cell viability assays. Oligonucleotides 81-96 BCL2 like 1 Homo sapiens 124-130 12063468-6 2002 Untreated cells and bcl-xl sense oligonucleotides were controls. Oligonucleotides 33-49 BCL2 like 1 Homo sapiens 20-26 12063468-8 2002 RESULTS: Bcl-xl protein expression after antisense oligonucleotides was downwardly regulated in both cell lines relative to sense oligonucleotides (>65%). Oligonucleotides 51-67 BCL2 like 1 Homo sapiens 9-15 12063468-8 2002 RESULTS: Bcl-xl protein expression after antisense oligonucleotides was downwardly regulated in both cell lines relative to sense oligonucleotides (>65%). Oligonucleotides 130-146 BCL2 like 1 Homo sapiens 9-15 12063468-12 2002 CONCLUSION: Antisense oligonucleotides directed at the bcl-xl gene product engender apoptosis in mesothelioma cell lines. Oligonucleotides 22-38 BCL2 like 1 Homo sapiens 55-61 11986224-7 2002 Finally, antisense bcl-x(L) and bcl-2 knockdown in T and B cells, respectively, and induction of Bcl-x(S) expression in granulocytes through antisense oligonucleotide-mediated redirection of bcl-x pre-mRNA splicing were sufficient to induce significant apoptosis in these cells. Oligonucleotides 151-166 BCL2 like 1 Homo sapiens 19-27 11986224-7 2002 Finally, antisense bcl-x(L) and bcl-2 knockdown in T and B cells, respectively, and induction of Bcl-x(S) expression in granulocytes through antisense oligonucleotide-mediated redirection of bcl-x pre-mRNA splicing were sufficient to induce significant apoptosis in these cells. Oligonucleotides 151-166 BCL2 like 1 Homo sapiens 97-102 11986224-7 2002 Finally, antisense bcl-x(L) and bcl-2 knockdown in T and B cells, respectively, and induction of Bcl-x(S) expression in granulocytes through antisense oligonucleotide-mediated redirection of bcl-x pre-mRNA splicing were sufficient to induce significant apoptosis in these cells. Oligonucleotides 151-166 BCL2 like 1 Homo sapiens 19-24 11792421-3 2002 By 18 h after the bcl-x antisense treatment, CEM cells showed over a 75% reduction in the levels of Bcl-xL protein and over 30% decreased viable cell counts compared with cells treated with the control oligonucleotide. Oligonucleotides 202-217 BCL2 like 1 Homo sapiens 18-23 11948488-6 2002 In a parallel approach, reduction of Bcl-x(L) protein by specific AS oligonucleotide (ISIS 16009) treatment enhanced the chemosensitivity of Mel Juso cells by 62% compared to cells treated with MM control oligonucleotide (ISIS 16967) as well as chemotherapy-induced apoptosis. Oligonucleotides 69-84 BCL2 like 1 Homo sapiens 37-45 11948488-6 2002 In a parallel approach, reduction of Bcl-x(L) protein by specific AS oligonucleotide (ISIS 16009) treatment enhanced the chemosensitivity of Mel Juso cells by 62% compared to cells treated with MM control oligonucleotide (ISIS 16967) as well as chemotherapy-induced apoptosis. Oligonucleotides 205-220 BCL2 like 1 Homo sapiens 37-45 11948488-8 2002 Reduction of Bcl-x(L) expression by AS oligonucleotides provides a rational and promising approach that may help to overcome chemoresistance in this malignancy. Oligonucleotides 39-55 BCL2 like 1 Homo sapiens 13-21 11874491-0 2002 Bcl-2 and bcl-xL antisense oligonucleotides induce apoptosis in melanoma cells of different clinical stages. Oligonucleotides 27-43 BCL2 like 1 Homo sapiens 10-16 11874491-3 2002 Primary cell cultures derived from 17 melanomas, the cell line A375, and normal melanocytes from healthy donors were treated with antisense oligonucleotides targeting either the bcl-xL mRNA or the bcl-2 and the bcl-xL mRNAs simultaneously. Oligonucleotides 140-156 BCL2 like 1 Homo sapiens 178-184 11874491-8 2002 As shown in A375 cells and the stage III melanoma cells 0513, both the bcl-xL monospecific oligonucleotide 4259 and the bcl-2/bcl-xL bispecific oligonucleotide 4625 effectively reduced tumor cell viability by induction of apoptosis with IC50 values ranging from 200 to 350 nM. Oligonucleotides 91-106 BCL2 like 1 Homo sapiens 71-77 11874491-8 2002 As shown in A375 cells and the stage III melanoma cells 0513, both the bcl-xL monospecific oligonucleotide 4259 and the bcl-2/bcl-xL bispecific oligonucleotide 4625 effectively reduced tumor cell viability by induction of apoptosis with IC50 values ranging from 200 to 350 nM. Oligonucleotides 144-159 BCL2 like 1 Homo sapiens 126-132 11278482-4 2001 Here we have targeted oligonucleotides antisense to the 5"-splice site of bcl-x(L), an anti-apoptotic gene that is overexpressed in various cancers, and shifted the splicing pattern of Bcl-x pre-mRNA from Bcl-x(L) to Bcl-x(S), a pro-apoptotic splice variant. Oligonucleotides 22-38 BCL2 like 1 Homo sapiens 205-213 11668508-0 2001 Bcl-x(L) antisense oligonucleotides induce apoptosis and increase sensitivity of pancreatic cancer cells to gemcitabine. Oligonucleotides 19-35 BCL2 like 1 Homo sapiens 0-8 11668508-3 2001 In this study, sequence-specific antisense oligonucleotides targeting the coding region of Bcl-x(L) were designed to examine whether apoptosis could be induced and chemosensitivity could be increased in pancreatic cancer cells. Oligonucleotides 43-59 BCL2 like 1 Homo sapiens 91-99 11668508-6 2001 In all examined pancreatic cancer cells, Bcl-x(L) expression was reduced after transfection of the antisense oligonucleotides. Oligonucleotides 109-125 BCL2 like 1 Homo sapiens 41-49 11668508-8 2001 Furthermore, Bcl-x(L) antisense oligonucleotides enhanced the cytotoxic effects of gemcitabine in pancreatic cancer cells. Oligonucleotides 32-48 BCL2 like 1 Homo sapiens 13-21 11668508-9 2001 Our results indicate that Bcl-x(L) antisense oligonucleotides effectively inhibited pancreatic cancer cell growth and caused apoptosis by reducing Bcl-x(L) protein levels. Oligonucleotides 45-61 BCL2 like 1 Homo sapiens 26-34 11668508-9 2001 Our results indicate that Bcl-x(L) antisense oligonucleotides effectively inhibited pancreatic cancer cell growth and caused apoptosis by reducing Bcl-x(L) protein levels. Oligonucleotides 45-61 BCL2 like 1 Homo sapiens 147-155 11668508-10 2001 Bcl-x(L) antisense oligonucleotides also increased the chemosensitivity of pancreatic cancer cells, suggesting that Bcl-x(L) antisense therapy might be a potential future approach in this disease. Oligonucleotides 19-35 BCL2 like 1 Homo sapiens 0-8 11668508-10 2001 Bcl-x(L) antisense oligonucleotides also increased the chemosensitivity of pancreatic cancer cells, suggesting that Bcl-x(L) antisense therapy might be a potential future approach in this disease. Oligonucleotides 19-35 BCL2 like 1 Homo sapiens 116-124 11458048-0 2001 Chemosensitization of bladder carcinoma cells by bcl-xL antisense oligonucleotides. Oligonucleotides 66-82 BCL2 like 1 Homo sapiens 49-55 11278482-4 2001 Here we have targeted oligonucleotides antisense to the 5"-splice site of bcl-x(L), an anti-apoptotic gene that is overexpressed in various cancers, and shifted the splicing pattern of Bcl-x pre-mRNA from Bcl-x(L) to Bcl-x(S), a pro-apoptotic splice variant. Oligonucleotides 22-38 BCL2 like 1 Homo sapiens 74-82 11278482-4 2001 Here we have targeted oligonucleotides antisense to the 5"-splice site of bcl-x(L), an anti-apoptotic gene that is overexpressed in various cancers, and shifted the splicing pattern of Bcl-x pre-mRNA from Bcl-x(L) to Bcl-x(S), a pro-apoptotic splice variant. Oligonucleotides 22-38 BCL2 like 1 Homo sapiens 185-190 11350916-6 2001 In contrast to many other anticancer agents to which the apoptotic response is decreased because of p53 mutations, our data suggest that the bcl-2/bcl-xL bispecific antisense oligonucleotide 4625 effectively induces p53-independent apoptosis in human C8161 melanoma cells. Oligonucleotides 175-190 BCL2 like 1 Homo sapiens 147-153 11431734-5 2001 Down-modulation of Bcl-xL by antisense oligonucleotide activated apoptosis in HepG2 cells in response to cellular stresses induced by staurosporine treatment or by serum starvation. Oligonucleotides 39-54 BCL2 like 1 Homo sapiens 19-25 11431734-6 2001 Ectopic expression of transcriptionally active p53 alone was not sufficient for the activation of apoptosis in p53-null Hep3B cells, but apoptosis was induced when endogenous Bcl-xL was simultaneously inhibited by antisense oligonucleotide in these cells. Oligonucleotides 224-239 BCL2 like 1 Homo sapiens 175-181 11350916-0 2001 p53-Independent induction of apoptosis in human melanoma cells by a bcl-2/bcl-xL bispecific antisense oligonucleotide. Oligonucleotides 102-117 BCL2 like 1 Homo sapiens 74-80 11350916-3 2001 Upon treatment with oligonucleotide 4625, p53-mut C8161 cells showed earlier DNA damage, which occurred concomitantly with the reduction of bcl-2 and bcl-xL expression and the increase in the expression of proapoptotic bax. Oligonucleotides 20-35 BCL2 like 1 Homo sapiens 150-156 11278482-4 2001 Here we have targeted oligonucleotides antisense to the 5"-splice site of bcl-x(L), an anti-apoptotic gene that is overexpressed in various cancers, and shifted the splicing pattern of Bcl-x pre-mRNA from Bcl-x(L) to Bcl-x(S), a pro-apoptotic splice variant. Oligonucleotides 22-38 BCL2 like 1 Homo sapiens 205-210 11278482-8 2001 These differences in responses to oligonucleotide treatment were analyzed in the context of expression of Bcl-x(L), Bcl-x(S), and Bcl-2 proteins. Oligonucleotides 34-49 BCL2 like 1 Homo sapiens 106-114 11278482-8 2001 These differences in responses to oligonucleotide treatment were analyzed in the context of expression of Bcl-x(L), Bcl-x(S), and Bcl-2 proteins. Oligonucleotides 34-49 BCL2 like 1 Homo sapiens 106-111 11085527-7 2000 The most active oligonucleotides of both types decreased the level of Bcl-xL protein expression to 5-30% of the control level. Oligonucleotides 16-32 BCL2 like 1 Homo sapiens 70-76 11114725-6 2000 Inhibition of Bcl-XL function by overexpression of Bax or administration of antisense oligonucleotides against Bcl-XL mRNA resulted in sensitization of Panc-1 cells to TRAIL and PancTuI cells to anti-CD95 antibody-induced cell death. Oligonucleotides 86-102 BCL2 like 1 Homo sapiens 14-20 11114725-6 2000 Inhibition of Bcl-XL function by overexpression of Bax or administration of antisense oligonucleotides against Bcl-XL mRNA resulted in sensitization of Panc-1 cells to TRAIL and PancTuI cells to anti-CD95 antibody-induced cell death. Oligonucleotides 86-102 BCL2 like 1 Homo sapiens 111-117 11259472-0 2001 Activity of a novel bcl-2/bcl-xL-bispecific antisense oligonucleotide against tumors of diverse histologic origins. Oligonucleotides 54-69 BCL2 like 1 Homo sapiens 26-32 11259472-2 2001 We recently reported that the bcl-2/bcl-xL-bispecific antisense oligonucleotide 4625 induces apoptosis in lung carcinoma cells. Oligonucleotides 64-79 BCL2 like 1 Homo sapiens 36-42 11259472-4 2001 METHODS: Oligonucleotide 4625-mediated inhibition of bcl-2 and bcl-xL expression in vitro was measured in breast carcinoma cells with the use of reverse transcription-polymerase chain reaction (PCR), real-time PCR, and western blotting. Oligonucleotides 9-24 BCL2 like 1 Homo sapiens 63-69 11259472-9 2001 RESULTS: In breast carcinoma cells, oligonucleotide 4625 treatment reduced bcl-2 and bcl-xL messenger RNA levels in a dose-dependent manner. Oligonucleotides 36-51 BCL2 like 1 Homo sapiens 85-91 11259472-10 2001 At 600 nM:, oligonucleotide 4625 reduced Bcl-2 and Bcl-xL protein levels to 25% (95% confidence interval [CI] = 16% to 34%) and 20% (95% CI = 14% to 26%), respectively, of the levels in untreated cells and it decreased viability in all cell lines mainly by inducing apoptosis. Oligonucleotides 12-27 BCL2 like 1 Homo sapiens 51-57 11259472-11 2001 In vivo, oligonucleotide 4625 statistically significantly inhibited the growth of breast and colorectal carcinoma xenografts by 51% (95% CI = 28% to 74%) and 59% (95% CI = 44% to 74%), respectively, relative to those treated with control oligonucleotide 4626; it also reduced Bcl-2 and Bcl-xL protein levels and induced tumor cell apoptosis. Oligonucleotides 9-24 BCL2 like 1 Homo sapiens 286-292 11259472-12 2001 CONCLUSION: The bcl-2/bcl-xL-bispecific antisense oligonucleotide 4625 merits further study as a novel compound for cancer therapy. Oligonucleotides 50-65 BCL2 like 1 Homo sapiens 22-28 11512155-4 2001 Recently developed antisense oligonucleotides with the ability to inhibit the expression of anti-apoptotic proteins, including Bcl-2, Bcl-xL, FLIP and surviving, have been shown to facilitate tumor cell apoptosis and sensitize tumor cells to cytotoxic treatments. Oligonucleotides 29-45 BCL2 like 1 Homo sapiens 134-140 11186002-0 2000 [Suppression of expression of bcl-2 and bcl-xL genes using antisense oligonucleotides: a new approach to cancer therapy]. Oligonucleotides 69-85 BCL2 like 1 Homo sapiens 40-46 10918201-2 2000 Here we describe the use of the 2;-O-methoxy-ethoxy antisense oligonucleotide 4259 targeting nucleotides 687-706 of the bcl-xL mRNA, a sequence that does not occur in the pro-apoptotic bcl-xS transcript, to restore apoptosis in estrogen-dependent and independent breast carcinoma cells. Oligonucleotides 62-77 BCL2 like 1 Homo sapiens 120-126 10918201-4 2000 Treatment of MCF7 cells with oligonucleotide 4259 at a concentration of 600 nM for 20 hr decreased bcl-xL mRNA and protein levels by more than 80% and 50%, respectively. Oligonucleotides 29-44 BCL2 like 1 Homo sapiens 99-105 10918201-6 2000 Moreover, oligonucleotide 4259 efficiently downregulated bcl-xL expression and decreased cell growth in the breast carcinoma cell lines T-47D, ZR-75-1, and MDA-MB-231. Oligonucleotides 10-25 BCL2 like 1 Homo sapiens 57-63 10873111-0 2000 A novel bispecific antisense oligonucleotide inhibiting both bcl-2 and bcl-xL expression efficiently induces apoptosis in tumor cells. Oligonucleotides 29-44 BCL2 like 1 Homo sapiens 71-77 10873111-4 2000 To test the possibility that oligonucleotides targeting this region have the potential to down-regulate bcl-2 and bcl-xL expression simultaneously, three 2"-O-methoxy-ethoxy-modified phosphorothioate oligonucleotides were designed. Oligonucleotides 29-45 BCL2 like 1 Homo sapiens 114-120 10873111-5 2000 These oligonucleotides differed in the number of mismatches to bcl-2 and bcl-xL and in the number of nucleotides to which the modifications were made. Oligonucleotides 6-22 BCL2 like 1 Homo sapiens 73-79 10873111-9 2000 This is the first report of a bcl-2/bcl-xL bispecific antisense oligonucleotide that deserves attention as a therapeutic compound in lung cancer and other malignancies in which bcl-2 and/or bcl-xL are overexpressed. Oligonucleotides 64-79 BCL2 like 1 Homo sapiens 36-42 10873111-9 2000 This is the first report of a bcl-2/bcl-xL bispecific antisense oligonucleotide that deserves attention as a therapeutic compound in lung cancer and other malignancies in which bcl-2 and/or bcl-xL are overexpressed. Oligonucleotides 64-79 BCL2 like 1 Homo sapiens 190-196 10545916-0 1999 Induction of endogenous Bcl-xS through the control of Bcl-x pre-mRNA splicing by antisense oligonucleotides. Oligonucleotides 91-107 BCL2 like 1 Homo sapiens 24-29 10545916-4 1999 We show here that altering the ratio of Bcl-xL to Bcl-xS in the cell using an antisense oligonucleotide permitted cells to be sensitized to undergo apoptosis in response to ultraviolet B radiation and chemotherapeutic drug treatment. Oligonucleotides 88-103 BCL2 like 1 Homo sapiens 40-46 10412646-3 1999 Thus, induction of apoptosis of vascular smooth muscle cells by p65 NF-kappa B and Bcl-xL antisense oligonucleotides or p53 overexpression could be useful for limiting vascular lesions associated with restenosis. Oligonucleotides 100-116 BCL2 like 1 Homo sapiens 83-89 10530711-11 1999 These include oligonucleotides that target the messages of the Bcl-X(L) and protein kinase-Calpha (PKCalpha) genes. Oligonucleotides 14-30 BCL2 like 1 Homo sapiens 63-71 10454803-0 1999 Sequence of Bcl-XL antisense oligonucleotides. Oligonucleotides 29-45 BCL2 like 1 Homo sapiens 12-18 9840921-2 1998 Administration of bcl-x-antisense oligonucleotides decreased Bcl-xL protein levels in the MKN-45 human gastric cancer cell line. Oligonucleotides 34-50 BCL2 like 1 Homo sapiens 18-23 10050882-7 1999 Downregulation of Bcl-X(L) to the same extent using antisense oligonucleotides enhanced etoposide-induced apoptosis by twofold. Oligonucleotides 62-78 BCL2 like 1 Homo sapiens 18-26 9840921-8 1998 In conclusion, we demonstrated that administration of bcl-x-antisense oligonucleotides or overexpression of Bak protein induces sensitization to apoptosis in MKN-45 gastric cancer cells, suggesting that endogenous Bcl-xL expression in cancer cells is an important modulator of apoptosis. Oligonucleotides 70-86 BCL2 like 1 Homo sapiens 214-220 10085086-4 1999 Treatment of neurons with an antisense oligonucleotide to bcl-2 mRNA or that to bcl-x mRNA blocked the up-regulation of Bcl-2 or Bcl-x expression, respectively, and partially inhibited the neuroprotective effect induced by TNF. Oligonucleotides 39-54 BCL2 like 1 Homo sapiens 129-134 9840921-2 1998 Administration of bcl-x-antisense oligonucleotides decreased Bcl-xL protein levels in the MKN-45 human gastric cancer cell line. Oligonucleotides 34-50 BCL2 like 1 Homo sapiens 61-67 9840921-8 1998 In conclusion, we demonstrated that administration of bcl-x-antisense oligonucleotides or overexpression of Bak protein induces sensitization to apoptosis in MKN-45 gastric cancer cells, suggesting that endogenous Bcl-xL expression in cancer cells is an important modulator of apoptosis. Oligonucleotides 70-86 BCL2 like 1 Homo sapiens 54-59 9525737-9 1998 Antisense oligonucleotides targeted to bcl-x downregulated the expression of Bcl-x, and increased the susceptibility of HL-60. Oligonucleotides 10-26 BCL2 like 1 Homo sapiens 39-44 9525737-9 1998 Antisense oligonucleotides targeted to bcl-x downregulated the expression of Bcl-x, and increased the susceptibility of HL-60. Oligonucleotides 10-26 BCL2 like 1 Homo sapiens 77-82 9461197-3 1998 Downregulation of intimal cell bcl-xL expression with the use of antisense oligonucleotides induced apoptosis and acute regression of vascular lesions. Oligonucleotides 75-91 BCL2 like 1 Homo sapiens 31-37 9185513-6 1997 Antisense oligonucleotide against bcl-x mRNA inhibited protective effect of LIF accompanied with the reduction in bclxL protein. Oligonucleotides 10-25 BCL2 like 1 Homo sapiens 34-39 9185513-6 1997 Antisense oligonucleotide against bcl-x mRNA inhibited protective effect of LIF accompanied with the reduction in bclxL protein. Oligonucleotides 10-25 BCL2 like 1 Homo sapiens 114-119