Abstract
Gastric cancer is the second most common cause of cancer deaths worldwide. The underlying molecular mechanisms of its carcinogenesis are relatively poorly characterized. Hedgehog (Hh) signaling, which is critical for development of various organs including the gastrointestinal tract, has been associated with gastric cancer. The present study was undertaken to reveal the underlying mechanism by which Hh signaling controls gastric cancer cell proliferation. Treatment of gastric cancer cells with cyclopamine, a specific inhibitor of Hh signaling pathway, reduced proliferation and induced apoptosis of gastric cancer cells. Cyclopamine treatment induced cytochrome c release from mitochondria and cleavage of caspase 9. Moreover, Bcl-2 expression was significantly reduced by cyclopamine treatment. These results suggest that Hh signaling regulates the survival of gastric cancer cells by regulating the expression of Bcl-2.
Highlights
Gastric cancer is the second most common cause of cancer deaths worldwide [1] and the 5-year relative survival rate remains poor [2]
The present study shows that Hh signaling regulates the survival of gastric cancer cells by regulating the expression of Bcl-2
To test whether Hh signaling is involved in the proliferation of gastric cancer cells, we blocked Hh signaling in SNU16 cells gastric cancer cells using cyclopamine, a specific inhibitor of Smo protein
Summary
Gastric cancer is the second most common cause of cancer deaths worldwide [1] and the 5-year relative survival rate remains poor [2]. The intestinal type is a well differentiated tumor, characterized by cohesive neoplastic cells that form gland-like tubular structures, and the diffuse type is a poorly differentiated tumor in which individual cells infiltrate and thicken the stomach wall [2]. The former is frequently accompanied by liver metastasis while the latter is frequently associated with peritoneal dissemination [2]. Experiments conducted on gastric cancer cells have shown that cyclopamine, which inhibits cellular responses to Shh signaling by binding to Smo, can inhibit the malignant growth of gastric cancer cells in vitro and in vivo. The present study shows that Hh signaling regulates the survival of gastric cancer cells by regulating the expression of Bcl-2
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