Liver cancer is one of the commonly detected malignancy and third highest cause of deaths caused by cancer worldwide. The current study investigated the effect of triethylsilyl resveratrol on HuH7 and hep3B cell proliferation and explored the underlying mechanism. The viability of HuH7 and hep3B cells was suppressed to 23 and 18%, respectively on exposure to 2 µM triethylsilyl resveratrol for 72 h. Triethylsilyl resveratrol treatment of HuH7 cells led to a prominent increase in expression of Atg-5, LC3B-II and Beclin proteins. In triethylsilyl resveratrol treated HuH7 cells expression of activated PI3K and Akt proteins showed a prominent decrease compared to the control cells. Moreover, p-mTOR protein expression was also suppressed in HuH7 cells on treatment with 2 µM triethylsilyl resveratrol. In triethylsilyl resveratrol treated cells a marked increase in ERK1/2 phosphorylation was observed compared to the control cells. Treatment with 2 µM triethylsilyl resveratrol for 72 h led to a significant (p < 0.05) increase in GFP-LC3B labelling in HuH7 cells compared to the control cells. Thus, triethylsilyl resveratrol reduced liver cancer cell viability through increase expression of proteins associated with autophagy. Moreover, it increased p-ERK1/2 expression and targeted activation of PI3K/Akt protein in HuH7 cells. Therefore, triethylsilyl resveratrol may be studied further as a promising therapeutic agent for treatment of liver cancer.
Keywords: anti-cancer; autophagy; chemotherapy; liver cancer; triethylsilyl resveratrol.
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