Antitumor activity of Pinoresinol in vitro: Inducing apoptosis and inhibiting HepG2 invasion

• Published in: Journal of functional foods Vol. 45; pp. 206 - 214
• Main Authors: Zhang, Yawen, Zhao, Haobin, Di, Yichao, Li, Qi, Shao, Dongyan, Shi, Junling, Huang, Qingsheng
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.06.2018; Elsevier
• Subjects: Antitumor activity; Apoptosis; Cell migration; HepG2; Pinoresinol; L02 cells; HepG2 cells; ICAM-1; E-cadherin; Pinoresinol; MMP; VCAM-1; Pin; HepG2; Antitumor activity; MMP-9; Cell migration; Apoptosis
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2018.04.009

Pin exhibits significant suppression on the growth of hepatoma cells in vitro. These effects were largely mediated via apoptosis associated with mitochondrial-mediated intrinsic pathways and the death receptor-mediated extrinsic pathway, as well as the disturbance of tubulin polymerization dynamics. In addition, Pin treatment increased the expression of E-cadherin and decreased the expression of VCAM-1, ICAM-1 and MMP-9 may also contribute to its function of anti-migration and invasion. [Display omitted] •Pinoresinol showed antitumor effects by inducing HepG2 apoptosis and inhibiting invasion. (+)-Pinoresinol (Pin), a biologically active lignan and widely found in many dietary plants, was reported to have antifungal, anti-inflammatory, antioxidation, and hypoglycemic activities. In the present study, the capability of Pin to inhibit human hepatocellular carcinoma HepG2 cells was evaluated and the mechanism was analyzed. Pin exhibited significant inhibition of HepG2 proliferation and revealed a pro-apoptotic effect. Pin led to activation of Fas, FasL, caspase-8, and Bid, which provoked death receptor apoptotic signals. Significant loss of mitochondrial membrane potential was also observed, as well as the altered expression of mitochondrial apoptotic proteins, including increased Cyto-c, Bax/Bcl-2 ratio, and caspase 3. Pin also exhibited inhibitory effect on the migration and invasion of HepG2 in a concentration-dependent manner by increasing E-cadherin and decreasing VCAM-1, ICAM-1 and MMP-9 expression. All the results indicated Pin could inhibit HepG2 via the induction of apoptosis through the death receptor pathway and/or mitochondrial pathway and the inhibition of invasion via disturbing the cytoskeleton.