Methods: The changes of intracellular Ca2+ ([Ca2+]i) in HCC cells were examined using this website the Ca2+-sensitive dye Fura-2 AM. The cell proliferation was estimated with MTT and Edu assays, and the cell migration and invasion were estimated with scratch wound and transwell

assays. Results: TGF-β (10 ng/ml) rapidly stimulated [Ca2+]i increases in normal liver cell LO2 and hepatocellular carcinoma cell HepG2. Both 2-APB, a blocker of canonical transient receptor potential channels (TRPC6), and KB, a blocker of Na+/Ca2+ exchanger (NCX1) partially inhibited TGF-β-induced [Ca2+]i increase in HepG2(P < 0.05), and 2-APB had more markedly inhibitory effect than KB. In the absence of extracellular Ca2+, TGF-β did not induce significant the change of [Ca2+]i in HepG2 cells. The further study showed that the mRNA and protein expression levels of NCX1 and TRPC6 were obviously increased in HepG2 after incubation with TGF-β

for 24 hours. TGF-β promoted the cell proliferation, migration, and invasion in HepG2 cells, which was partially IDH inhibition inhibited by both 2-APB and KB. Bapta-am, an intracellular calcium chelator, completely inhibited the effect of TGF-β on HepG2 cells. Conclusion: TGF-β regulates the cellular behavior of HCC through intracellular Ca2+ signal. TRPC6 and NCX1 were involved in the role of TGF-β on HCC cells. Key Word(s): 1. TGF-β; 2. HCC; 3. NCX1; 4. TRPC6; Presenting Author: BIGUANG TUO Additional Authors: RUI XIE, JINGYU XU, GUORONG WEN, HAI JIN, XUEMEI LIU, YUAN YANG, BEI JI, YIXIA JIANG, HUI DONG Corresponding Author: BIGUANG TUO Affiliations: Department of Gastroenterology, Affiliated Hospital of Zunyi Medical college Objective: P2Y2 receptor (P2Y2R) mediates a variety selleck kinase inhibitor of biological functions. ATP is a physiologic ligand for P2Y2R, which can be released from inflammatory cells and tumor cells, and is an abundant biochemical component of the tumor microenvironment. It is well known

that chronic inflammation plays a key role in the development and progression of human hepatocellular carcinoma (HCC). In this study, we investigated the expression and role of P2Y2R in human HCC cells, which aimed to find a new therapeutic target against HCC. Methods: The experiments were performed in native isolated human HCC cells and normal hepatocytes, and human HCC cell lines. The xenograft model of human HCC was established in nude mice. Results: The mRNA and protein expressions of P2Y2R, not P2Y4R, in native human HCC cells and human HCC cell lines, HepG2 and BEL-7404, were markedly increased, compared to human normal hepatocytes and normal hepatocyte line LO2, respectively (P < 0.01 and P < 0.001). P2Y2R anatgonist suramin and specific siRNA, not P2Y4R specific siRNA, inhibited ATP-induced [Ca2+]i increases in HCC cells (P < 0.0001).