Methanol Extract of Nervilia Fordii Induces Apoptosis of Nasopharyngeal Carcinoma CNE-2 Cells Through ERK Signaling Pathway

OBJECTIVE To investigate the apoptosis effect and mechanism of Nervilia fordii methanol extracts(NFME) on nasopharyngeal carcinoma CNE-2 cells in vitro. METHODS The growth inhibition rate of CNE-2 cells treated with different concentrations of NFME(0, 0.25, 0.5, 1, 2, 3 mg·mL^-1) for 24, 48 h were detected by MTT. The effect of NFME on CNE-2 cell clone formation rate was observed by clonal test. The effect of NFME on CNE-2 cell apoptosis was observed by Hoechst apoptosis staining. The changes of phosphorylation level of caspase-3, ERK1/2 and c-Raf were detected by Western blotting. RESULTS The results of the MTT experiment showed that, compared with the control group, 0.5 mg·mL^-1 of NFME could inhibit the proliferation of CNE-2 cells at 24 h(P<0.05), and the inhibition rate reached 12.64%. At 48 h, 0.25 mg·mL^-1 of NFME could inhibit the proliferation of CNE-2 cells(P<0.05), and the inhibition rate reached 22.43%. The experiment of clonal ability showed that 0.25 mg·mL^-1 of NFME could inhibit CNE-2 formation of cell colonies(P<0.05). Hoechst33258 apoptosis staining observed that 0.25 mg·mL^-1 of NFME induced apoptosis in CNE-2 cells for 24 h(P<0.05), and the apoptosis rate reached 17.91%. The results of Western blotting showed that 0.5 mg·mL^-1 of NFME caused caspase-3 to shear in CNE-2 cells, and the shear effect became more pronounced as the concentration of drug was increased(P<0.01). Meanwhile, NFME could cut down the phosphorylation level of ERK1/2 and c-Raf in CNE-2 cells at 0.5 mg·mL^-1(P<0.05). CONCLUSION NFME can inhibit nasopharyngeal carcinoma CNE-2 cells and induce apoptosis, its mechanism may be related to the inhibition of ERK signaling pathway.