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.
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.
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.
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.