Curcumin L6H4 can significantly inhibit the proliferation and induce the apoptosis of BGC-823 cells, thus enhancing the expression levels of p53, p21, Bax, and Bcl-2 noticeably in vivo and in vitro.
Collectively, the results indicated that STC1 may serve an oncogenic role in hypoxic GC via dysregulating Bcl‑2, indicating that STC1 may be a potential therapeutic target in the treatment of GC.
Despite not increasing the intercellular ROS levels in gastric cancer cells, chaetocin did cause a reduction in mitochondrial membrane potential probably through its regulation on the expression of Bcl-2 and BAX.
The present findings indicate that DAP3 deficiency-induced chemoresistance in gastric cancer is at least partially mediated through the β-catenin/LGR5/Bcl-2 axis.
Although certain markers, including HER2, VEGER-2, ERCC1 and Bcl-2, have been utilized in clinical practise to screen out new patients with GC, the results of using these markers remains poor.
Knock-down of Uba2 inhibited GC cell proliferation, induced cell cycle arrest, and altered expression of cyclin D1, P21, P27, and Bcl-2, while up-regulation of Uba2 showed the opposite effects.
In conclusion, the results of the present study indicate the involvement of TFs in MDR in GC, and suggest that HNF-4α may enhance MDR in GC by regulating cell apoptosis and Bcl-2 expression.
PA induced cell apoptosis by regulating the expressions of apoptosis-related proteins (caspase-3, PARP, Bcl-2, and Bax) and suppressing the mitochondrial capacity of GC cell lines in vitro in a dose-dependent manner.
Thus, we found that HIF-1α is closely associated with MDR in GC and that HIF-1α may suppress MDR1/P-gp, LRP and Bcl-2 expression by inhibiting miR-27a expression.
This newly identified miRNA-135a-5p-AP-2α-BCL-2 pathway provides insight for the treatment of gastric cancer and solution for insensitivity of gastric cancer to chemotherapy drugs.
After ZNF139-siRNA was transfected into MKN28, ZNF139 expression in GC cells was inhibited by 90%; inhibition rate of 5-FU, L-OHP to tumor cells increased, and expressions of MDR1/P-gp, MRP1 and Bcl-2 were down-regulated, while Bax was up-regulated.
In this study, we assessed annexin A3 expression in 80 patients with gastric cancer and explore its correlation with prognosis Moreover, correlations with Ki-67, Bcl-2 and Bax were also investigated.
Altogether, these findings suggest that modulation of aberrant expression of miR-204, which in turn releases oncogenic Bcl-2 protein activity might hold promise for preventive and therapeutic strategies of GC.
Our results demonstrate that STAT3, but not STAT5, is involved in GC cell growth and cell cycle progression through regulation of gene expression, such as Bcl-2, p16(ink4a) and p21(waf1/cip1).
There were positive correlations between expressions of STAT3, survivin, Bcl-2 and pSTAT3 in gastric cancer, whereas there was negative correlation between STAT3 expression and SOCS-1 expression in gastric cancer.
These results indicate that RON-targeted siRNA could be therapeutically efficacious by inducing cell apoptosis through the modulation of the NF-kappaB and Bcl-2 family in gastric cancer cells.