Inhibition of EZH2 via the STAT3/HOTAIR signalling axis contributes to cell cycle arrest and apoptosis induced by polyphyllin I in human non-small cell lung cancer cells

Abstract

Objective: To explore the potential mechanism of polyphyllin I (PPI)-induced apoptosis in lung cancer cells.

Methods and materials: The pathological changes in lung cancer tissues and paracancerous tissues were first analysed by H&E staining and IHC staining. After PPI treatment, cell viability and apoptosis were detected by MTT assays, cell cycle analyses and flow cytometry. The expression levels of EZH2 and apoptosis-related molecules were evaluated by qRT-PCR and Western blotting.

Results: EZH2 overexpression decreased proapoptotic proteins, and this effect was reversed by PPI. Knockdown of HOTAIR downregulated EZH2 expression, upregulated proapoptotic proteins, and enhanced the effect of PPI treatment. Moreover, knockdown of STAT3 could counteract the effect of HOTAIR overexpression, which significantly increased the expression of EZH2, thus facilitating cell apoptosis in lung cancer.

Conclusions: PPI induced cell cycle arrest and apoptosis in lung cancer by inhibiting EZH2 through the STAT3/HOTAIR signalling pathway.

Keywords: Apoptosis; EZH2; Non-small cell lung cancer cells; Polyphyllin I; STAT3/HOTAIR signalling.