Shikonin inhibits proliferation, migration, invasion and promotes apoptosis in NCI-N87 cells via inhibition of PI3K/AKT signal pathway.

Shikonin has been testified to wield the anti-tumor action in multiple cancers. But, the clout of Shikonin for gastric cancer (GC) is still inconclusive. The contemplation of this research undertook to disclose the impacts of Shikonin on GC progress meanwhile to uncover the conceivable mechanism. NCI-N87 cells were disposed by Shikonin at diverse concentration points. The trials of CCK-8, colony formation, flow cytometry and Transwell assays were executed for detecting the functions of Shikonin in NCI-N87 cells. The impacts of miR-195 on Shikonin-regulated PI3K/AKT pathway were estimated via western blot. The in vivo trial was detected by xenografts model assay. We found that Shikonin suppressed cell survival and triggered apoptosis in NCI-N87 cells. Additionally, Shikonin restrained cell migration, invasion and down-regulated MMP2, RhoA, ROCK1 and Vimentin expression in NCI-N87 cells. Furthermore, Shikonin notably inhibited PI3K/AKT signal pathway, but the restraining functions were repealed by miR-195 inhibition in NCI-N87 cells. The in vivo trial results revealed that Shikonin determinately impeded tumor formation. In conclusion, these results demonstrated that Shikonin prohibited NCI-N87 cells proliferation, migration, invasion, and accelerated apoptosis by inactivation of PI3K/AKT pathway. The findings maybe provide a fresh opinion for healing GC.