Decanoic Acid Exerts Its Anti-Tumor Effects via Targeting c-Met Signaling Cascades in Hepatocellular Carcinoma Model

SIMPLE SUMMARY: Hepatocellular carcinoma (HCC) is a primary liver malignancy that remains a fatal disease with limited therapeutic options. Aberrant activation of c-Met can modulate tumor growth and progression in HCC. Herein, we have examined the anti-neoplastic effects of decanoic acid (DA) in hepatocellular carcinoma cells and in vivo mouse models. DA suppressed the phosphorylation of c-Met and induced apoptosis in HCC cells by inhibiting the expression of various oncogenic proteins. Moreover, DA inhibited the c-Met cascade in the preclinical cancer model. These results support the idea that DA can be considered a new anti-tumor agent for HCC. ABSTRACT: DA, one of the medium-chain fatty acids found in coconut oil, is suggested to have diverse biochemical functions. However, its possible role as a chemoprevention agent in HCC has not been deciphered. Aberrant activation of c-Met can modulate tumor growth and progression in HCC. Here, we report that DA exhibited pro-found anti-tumor effects on human HCC through the suppression of HGF/c-Met signaling cascades in vitro and in vivo. It was noted that DA inhibited HGF-induced activation of c-Met and its downstream signals. DA induced apoptotic cell death and inhibited the expression of diverse tumorigenic proteins. In addition, DA attenuated tumor growth and lung metastasis in the HCC mouse model. Similar to in vitro studies, DA also suppressed the expression of c-Met and its downstream signals in mice tissues. These results highlight the substantial potential of DA in the prevention and treatment of HCC.