The AT1/Raf/ERK1/2 signaling pathway is involved in Angiotensin II-enhanced proliferation of hepatic carcinoma cells

Angiotensin II (Ang II) has been strongly associated with biological behavior in human malignant tumors; nevertheless, its function in hepatic carcinoma growth and progression is still not well understood. This study investigates the effect and mechanism of Ang II on the HepG2 and Hep3B hepatic carcinoma cell lines in vitro. The effect of Ang II on HepG2 and Hep3B cell viability was examined by cell counting kit-8 assay (CCK-8). Quantitative real-time PCR and Western blot analysis detected the expression of angiotensin type 1 and type 2 receptors (AT1 and AT2), total extra-cellular signal-regulated kinases 1/2 (ERK1/2), phospho-ERK1/2 (p-ERK1/2) and Bcl-2 and c-Myc. Ang II significantly promoted HepG2 cell proliferation by affecting AT1 and AT2 expression and induced ERK1/2 pathway activation. This was reversed by treating HepG2 and Hep3B cells with AT1 blockers; candesartan, Raf inhibitor sorafenib, and ERK1/2 inhibitor PD98059. Ang II also up-regulated the expression of Bcl-2 and c-Myc in HepG2 cells, and our results suggest that Ang II has a positive role in HepG2 and Hep3B cell proliferation through the AT1/Raf/ERK1/2 signaling pathway.