An orally antitumor chalcone hybrid inhibited HepG2 cells growth and migration as the tubulin binding agent.

Liver cancer is a kind of high mortality cancer due to the difficulty of early diagnosis. It is necessary to develop the anticancer agents to treat liver cancer. Here, a novel chalcone derivative was synthesized and evaluated for anticancer activity in vitro against liver cancer cell lines (HepG2, SNU-423, SMMC7221, and SNU-398). The chalcone hybrid 9 displayed the antiproliferative effect against HepG2, SNU-423, SMMC7221 and SNU-398 cells with IC50 values of 0.9 μM, 2.7 μM, 6.2 μM and 4.6 μM, respectively. Cellular mechanisms showed that derivative 9 could obviously inhibit HepG2 cells growth and colony formation in a concentration-dependent manner. Analogue 9 inhibited the migration by regulating the expression levels of migration-releated markers and transcription factors (Snail and Slug). Tubulin polymerization inhibition assay illustrated that chalcone hybrid 9 might be a potent tubulin polymerization inhibitor. Importantly, compound 9 displayed the antitumor activity against liver cancer HepG2 cells in vivo with the low toxicity toward mice. Therefore, compound 9 as a novel tubulin polymerization inhibitor deserves further investigation to treat liver cancer. Graphical abstract Compound 9 displayed the antitumor activity against liver cancer HepG2 cells in vivo and low toxicity toward mice Figure: Orally antitumor chalcone hybrid 9 inhibited HepG2 cells growth and migration as the tubulin binding agent.