Inhibitory effect of icaritin on proliferation, migration, and invasion of human nasopharyngeal carcinoma cell CNE2 by regulating STAT3 activation.

Abstract

The influence of icaritin on the proliferation, migration, and invasion of human nasopharyngeal carcinoma cell CNE2 and the influencing mechanisms were discussed. Results indicated that icaritin can realize dosage-dependent inhibition of CNE2 cell proliferation, migration, and invasion and inhibit the expression levels of VEGF, KDR, bFGF, MMP2, and MMP9. It can also inhibit STAT3 phosphorylation without affecting STAT3 expression. Icaritin exerts multiple bonding effects on the SH2 structural domain of STAT3. Therefore, icaritin can become a candidate drug for resisting nasopharyngeal carcinoma, and its mechanism is related to the blocking of STAT3 signaling pathway activation.