MCL1 is an antiapoptotic member of the BCL-2 family that has been found to play an essential role in advancing chemoresistance and could be a promising target for the treatment of ovarian cancer.
Here, we demonstrated that Qu evoked ER stress to involve in mitochondria apoptosis pathway via the p-STAT3/Bcl-2 axis in OC cell lines and in primary OC cells.
MTT assay, caspase-3 activity assay, and flow cytometry analysis were conducted to investigate the effects of NEAT1, miR-34a-5p, or B-cell lymphoma-2 (BCL2) on OC cell proliferation and apoptosis.
In the present study, as a novel autophagy regulator, BCL2‑associated athanogene 3 (BAG3) was investigated to study its role in cisplatin sensitivity in epithelial ovarian cancer.
In addition, luciferase reporter assay and qRT-PCR were conducted to verify whether the Bcl-2-associated athanogene 5 (BAG5) gene was the downstream target of miR-127-3p in EOC.
The reversal ratios of 1 μg/ml sCD40L combined with cisplatin in SKOV3 and SKOV3/DDP cells were 2.11, 2.71, while the reversal ratios of 2 μg/ml sCD40L combined with cisplatin in SKOV3 and SKOV3/DDP cells were 3.78, 5.20, respectively. sCD40L or sCD40L combined cisplatin increased tumor cells in G0/G1 phase. sCD40L in combination with cisplatin decreased the expression levels of GST-π, LRP, Survivin, p53 and Bcl-2 in both epithelial ovarian cancer cell lines.
This study underscores an essential role of SIRT3 in the antitumor effect of Bcl-2 inhibitors in human ovarian cancer through regulating both metabolism and apoptosis.
Collectively, these results indicate that pharmacological inhibitors or genetic knockdown of Bcl-2 may be a potential strategy for improving cisplatin treatment of ovarian cancer.
In summary, calycosin might exert anti-growth and induce-apoptosis activity against ovarian cancer SKOV3 cells through activating caspases and Bcl-2 family proteins, therefore presenting as a promising therapeutic agent for the treatment of ovarian cancer.
This study assesses TRAIL-R2 (TNF-related apoptosis-inducing ligand receptor 2) and BCL2 (B cell CLL/lymphoma 2) expression as well as CpG island methylation within the TRAIL-R2 promoter in ovarian serous tumors and primary and metastatic serous EOC (epithelial ovarian cancer).
The combined treatment with BLU and gemcitabine further activated p53 and p21 expression, whereas the productions of Bcl-2, Bcl-xL, and nuclear factor-kappa B proteins were decreased, with BLU possibly being more effective in the treatment of ovarian cancer when given in combination with gemcitabine, rather than as a single agent.
The data presented here show that Stattic restored the sensitivity to cisplatin in chemoresistant ovarian cancer by significant reductions in the expression of the anti-apoptosis protein Bcl-2, Bcl-XL, Survivin protein and phosphorylated-Akt levels.
The observations made in the present study suggest that alterations in expression of the Fas family and the Bcl-2 family members occur and play a key role in the deregulated growth of epithelial ovarian cancer.
We investigated the role of major Fas and Bcl-2 family members as predictors of response to platinum-based chemotherapy in epithelial ovarian cancer (EOC).