The root of Actinidia chinensis, as traditional Chinese medicine, has been shown to inhibit cell proliferation in numerous cancer cells. However, the mechanisms underlying its inhibitory activity remain unclear. Death rates of hepatocellular carcinoma (HCC) are increasing, but therapies for advanced HCC are not well developed. We choose the extract from root of Actinidia chinensis (ERAC) to treat the HCC cell lines in vitro, displaying distinct effects on cell proliferation, S-phase cell cycle arrest, and apoptosis. LAMB3, the gene encoding laminin subunit beta-3, plays a key role in the proliferation suppression and S-phase cell cycle arrest of HepG2 cells treated with ERAC. The downstream genes ITGA3, CCND2, and TP53 in LAMB3 pathway show the same response to ERAC as LAMB3. Thus, LAMB3 pathways, along with extracellular matrix-receptor interaction, pathways in cancer, and focal adhesion, are involved in the ERAC-induced suppressive response in HepG2.
Keywords: Actinidia chinensis; Hepatocellular carcinoma; LAMB3.