Candesartan attenuates angiogenesis in hepatocellular carcinoma via downregulating AT1R/VEGF pathway

Area of Science:

• Oncology
• Cardiovascular Research
• Molecular Biology

Background:

• Angiotensin II type 1 receptor (AT1R) is implicated in tumor progression and angiogenesis.
• AT1R expression is observed in various tumor types, including liver cancer.
• Targeting AT1R may offer a novel therapeutic strategy for hepatocellular carcinoma (HCC).

Purpose of the Study:

• To investigate AT1R expression in HCC tissues.
• To evaluate the antitumor effects of the AT1R antagonist Candesartan in liver cancer models.
• To elucidate the role of AT1R in regulating VEGF-A production and angiogenesis in HCC.

Main Methods:

• Analysis of AT1R and VEGF-A expression, and microvascular density (MVD) in HCC patient samples.
• In vitro experiments assessing the effects of Angiotensin II and Candesartan on liver cancer cell proliferation and VEGF-A production.
• In vivo studies using mouse xenograft models to evaluate Candesartan's impact on tumor growth, angiogenesis, and VEGF-A expression.

Main Results:

• AT1R expression positively correlated with VEGF-A and MVD in HCC patients.
• Angiotensin II upregulated AT1R and VEGF-A production in liver cancer cells dose-dependently.
• Candesartan reversed Angiotensin II-induced effects in vitro and inhibited tumor growth and angiogenesis in vivo by downregulating VEGF-A.

Conclusions:

• AT1R plays a role in promoting angiogenesis in liver cancer.
• Candesartan demonstrates potential as an anti-angiogenic agent for treating HCC.
• Targeting the AT1R-VEGF-A axis may be a viable strategy to suppress liver cancer progression.