AI Article Synopsis
- Bcl-2 is an anti-apoptotic protein that interacts with Beclin1, an important player in autophagy, but its role in autophagy regulation is unclear.
- In experiments with SGC-7901 cells that overexpress Bcl-2, knocking down Bcl-2 using siRNA downregulated its levels by about 82% and induced autophagy, increasing Beclin1 protein by 58%.
- The study shows that targeting Bcl-2 can enhance autophagy without triggering apoptosis, suggesting that Bcl-2 siRNA could be a potential therapeutic strategy for treating gastric cancer cells that have high levels of Bcl-2.
Article Abstract
While Bcl-2 protein is involved in the regulation of apoptosis, recent research showed that Beclin1, described as the essential autophagy effector and haploinsufficient tumor suppressor, was originally isolated as a Bcl-2 interacting protein. Beclin1 interacts with Bcl-2 through a BH3 domain; nevertheless, the function of the anti-apoptotic gene, Bcl-2, in autophagy is not well understood. We explored the role of Bcl-2 in autophagy in human SGC-7901 cells in which Bcl-2 is overexpressed. Knockdown of Bcl-2 by small interfering RNA in human SGC-7901 cells downregulated Bcl-2 protein levels ∼82% and induced autophagy. Beclin1 protein, the first identified autophagy gene product, was induced by as much as 58%. Transmission electron microscopy and DNA fragmentation assay showed that autophagy was enhanced, but not apoptosis, in Bcl-2 siRNA treated cells. The results provide evidence that knockout the anti-apoptotic gene Bcl-2 induces autophagy in SGC-7901 cells and Bcl-2 specific siRNA may be used as a potential therapeutic strategy in gastric cancer cells that overexpress Bcl-2.
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| http://dx.doi.org/10.1002/cbin.10333 | DOI Listing |
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