Scutellarin-induced apoptosis in HepG2 hepatocellular carcinoma cells via a STAT3 pathway.

Liver cancers remain one main reason for the mortality in patients with tumors. Up to now, however, the effective drugs to treat liver cancers are limited. The aim of this study was to study whether Scutellarin which was widely found in many medicinal plants can exert an inhibitory role in HepG2 hepatocellular carcinoma cell lines, and to explore its molecular mechanisms. The MTT assay showed that Scutellarin markedly inhibited the proliferation of HepG2 cells in a concentration- and time-dependent manner. Moreover, Scutellarin-treated cells exhibited typical apoptotic appearance by staining assay. Also, Scutellarin-treated HepG2 cells exhibited the reduction of ROS production, compared with untreated HepG2 cells. Western blot analysis displayed that STAT3 protein was obviously decreased in Scutellarin-treated HepG2 cells. Furthermore, STAT3 transcriptional targets Bcl-XL and Mcl-1 were also downregulated in HepG2 cells treated by Scutellarin. In summary, we found that Scutellarin was able to inhibit the proliferation and induce the apoptosis of HepG2 cells via a STAT3 signal pathway, which provided evident support for developing Scutellarin as an alternative treatment for liver cancer.