Vitamin D3 regulates cell viability in gastric cancer and cholangiocarcinoma / 대한해부학회지

A low serum level of vitamin D has been associated with an increased incidence of gastrointestinal tract cancers. However, the effects of vitamin D3 have not been investigated in gastric cancer and cholangiocarcinoma. In the present study, we found that vitamin D3 treatment significantly suppressed the viability of gastric cancer and cholangiocarcinoma cells. Moreover, vitamin D3 had a synergistic effect with other anti-cancer drugs, such as paclitaxel, adriamycin, and vinblastine, for suppressing cell viability. To determine the underlying mechanism involved in the regulation of viability by vitamin D3, we examined the effects of vitamin D3 on expression of hedgehog signaling target genes, which has been associated with gastric cancer and cholangiocarcinoma. Vitamin D3 treatment decreased the level of mRNA expression of patched1, Gli1, cyclin D1, and Bcl2, suggesting the possibility that vitamin D3 may act through regulation of hedgehog signaling. From the above results, we conclude that vitamin D3 regulates cell viability in gastric cancer and cholangiocarcinoma.

CDH3/P-Cadherin regulates migration of HuCCT1 cholangiocarcinoma cells / 대한해부학회지

Intrahepatic cholangiocarcinoma is the second most common subtype of primary hepatobilliary cancer. Despite advances in surgical and medical therapy, its survival rate remains poor. Compared to hepatocellular carcinoma (HCC), the most common liver malignancy, the underlying mechanisms of cholangiocarcinoma carcinogenesis are poorly characterized. P-cadherin (CDH3) is a cadherin super family member. Although CDH3 is frequently over-expressed in cholangiocarcinoma tissues, its roles have never been characterized. To determine the roles of CDH3 in cholangiocarcinoma, we investigated CDH3 function in HuCCT1 cells using specific siRNA. Transfection with CDH3 siRNA did not affect proliferation of HuCCT1 cells. However, cell migration and invasion were significantly reduced when CDH3 was down-regulated. In addition, expressions of several biomarkers for epithelial-mesenchymal transition (EMT) were not changed by CDH3 down-regulation. These results suggest that CDH3 regulates cell migration independent of EMT in cholangiocarcinoma cells.