BCL2, BCL2 apoptosis regulator, 596

N. diseases: 1456; N. variants: 27
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE We analysed the transcript expression of CLEC5A in glioblastoma by accessing The Cancer Genome Atlas (TCGA). qRT-PCR was performed to detect the RNA expression of genes in cells and tissues, and Western blot was used to measure the protein levels (Cyclin D1, Bcl-2, BAX, PCNA, MMP2, MMP9, Akt and Akt phosphorylation) in tissues and cells. 30834619 2019
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Therefore, we combined ITs (9.2.27-PE38KDEL or Mel-14-PE38KDEL) targeting chondroitin sulfate proteoglycan 4 (CSPG4) with a panel of Bcl-2 family inhibitors (ABT-737, ABT-263, ABT-199 [Venetoclax], A-1155463, and S63845) against patient-derived glioblastoma, melanoma, and breast cancer cells/cell lines. 30625226 2019
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Accumulating evidence indicates that resistance to apoptosis in GB is mediated via upregulation of pro-survival BCL2-family members. 30389373 2019
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE In this study, we examined whether inhibition of the anti-apoptotic Bcl-2 family proteins Bcl-2 and Bcl-xL enhances the biological effects of the repurposed CUSP9 regimen in an in vitro setting of glioblastoma. 31222722 2019
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Elevated ZHX1 expression correlated with poor prognosis in GBM patients, and in vitro studies demonstrated that ZHX1 attenuated GBM cell apoptosis by downregulation of pro-apoptotic protein (Bax) and upregulation of anti-apoptotic protein (Bcl-2). 31648104 2019
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Treatment with a Bcl2 inhibitor does not fully explain the effect of gossypol on glioblastoma. 31658771 2019
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Our data indicate that concomitant inhibition of RAC1 and Bcl-2/Bcl-xL induces pro-apoptotic and anti-migratory glioblastoma phenotypes as well as synergistic anti-neoplastic activities. 30859392 2019
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Taken together, our findings demonstrate that KPNB1 is required for proteostasis maintenance and its inhibition induces apoptosis in glioblastoma cells through UPR-mediated deregulation of Bcl-2 family members. 29520102 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Furthermore, the expression levels of the Bcl-2 anti-apoptotic protein was significantly decreased while Bax and caspase-3 expression were both increased in glioblastoma cells (all, p<0.05). 29940755 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE We previously developed cell-penetrating VDAC1-derived peptides that interact with hexokinase (HK), Bcl-2, and Bcl-xL to prevent the anti-apoptotic activities of these proteins and induce cancer cell death, with a focus on leukemia and glioblastoma. 29698587 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Our data reported that ASA affected GBM-EC viability, tube-like structure formation, cell migration, and VEGF releasing in a dose-dependent manner and that combined treatments with TMZ, BEV, and SUN synergized to counteract proangiogenic cell ability. mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1α, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN. 30144594 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Recent data suggest that glioblastomas (GBM) activate the c-MET signaling pathway and display increased levels in anti-apoptotic Bcl-2 family members. 29743557 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE MAO-B inhibitors selegiline and rasagiline protect neurons via increase expression of anti-apoptotic Bcl-2 and pro-survival neurotrophic factors in human neuroblastoma SH-SY5Y and glioblastoma U118MG cell lines. 29279995 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE The inhibition of both SH-SY5Y and U87MG cell proliferation was associated with an increase in the thiosulfate level, the number of cells with the inactive form of Bcl-2 protein, and with a decrease of mitochondrial membrane potential. 29508061 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE CTRP8-induced RXFP1 activation caused an increase in cellular protein levels of the anti-apoptotic Bcl members and STAT3 targets Bcl-2 and Bcl-XL in human GBM. 29949238 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Dual Inhibition of Bcl-2/Bcl-xL and XPO1 is synthetically lethal in glioblastoma model systems. 30337641 2018
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Type B and A monoamine oxidase and their inhibitors regulate the gene expression of Bcl-2 and neurotrophic factors in human glioblastoma U118MG cells: different signal pathways for neuroprotection by selegiline and rasagiline. 28577058 2017
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE These results raise the question of whether Bcl-2 and XIAP genes can be responsible for the inhibition of programmed cell death in glioblastomas. 29236891 2017
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Our results revealed that the Au PENPs were capable of delivering Bcl-2 siRNA to glioblastoma cells with an excellent transfection efficiency, leading to specific gene silencing in the target cells (22% and 25.5% Bcl-2 protein expression in vitro and in vivo, respectively) thanks to the RGD peptide-mediated targeting pathway. 27921110 2017
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Our findings uncover a novel mechanism through which mitochondrial PKM2 phosphorylates Bcl2 and inhibits apoptosis directly, highlight the essential role of PKM2 in ROS adaptation of cancer cells, and implicate HSP90-PKM2-Bcl2 axis as a potential target for therapeutic intervention in glioblastoma. 28035139 2017
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Bcl-2 and the closely related Bcl-xL and Mcl-1 are often overexpressed in glioblastoma cells. 26775694 2016
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE MicroRNA-138 promotes acquired alkylator resistance in glioblastoma by targeting the Bcl-2-interacting mediator BIM. 26887050 2016
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 AlteredExpression disease BEFREE Hypoxic regions of GBM also highly express the pro-cell death Bcl-2 family member BNIP3, yet when BNIP3 is overexpressed in glioma cells, it induces cell death. 26467103 2016
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE In conclusion, this study suggested that miR-206 could act as a tumor suppressor gene through inhibiting BCL-2 in the development of glioblastoma. 27558109 2016
CUI: C0017636
Disease: Glioblastoma
Glioblastoma
0.100 Biomarker disease BEFREE Our data suggest that Bcl-2 confers resistance to mTORC1/2 inhibitors in TP53 wild type GSCs and that combined inhibition of both mTORC1/2 and Bcl-2 is worthwhile to explore further in TP53 wild type glioblastomas, whereas in TP53 mutated glioblastomas dual mTORC1/2 inhibitors should be explored. 27533080 2016