Key result
Angiotensin II significantly promoted the proliferation of HepG2 and Hep3B hepatic carcinoma cells in vitro through the AT1/Raf/ERK1/2 signaling pathway.
Why the study?
Does Angiotensin II promote proliferation in human hepatic carcinoma cell lines?
Does Angiotensin II promote proliferation in human hepatic carcinoma cell lines?
p-value: p=<0.05
Angiotensin II promotes hepatic carcinoma cell proliferation in vitro via the AT1/Raf/ERK1/2 signaling pathway, highlighting a potential therapeutic target for primary liver cancer.
Does not support clinical use of AT1 inhibitors in HCC; leaves open whether pathway blockade improves outcomes in vivo.
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.
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Qi et al. (2018) studied Hepatic carcinoma. Angiotensin II vs. Control was evaluated on Cell viability and proliferation (p=<0.05). Angiotensin II significantly promoted the proliferation of HepG2 and Hep3B hepatic carcinoma cells in vitro through the AT1/Raf/ERK1/2 signaling pathway.
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