Cynaropicrin inhibits lung cancer proliferation by targeting EGFR/AKT signaling pathway

Purpose: To investigate the anti-proliferative effect of cynaropicrin on lung cancer cell lines, and the underlying molecular mechanism. Methods: The effect of cynaropicrin treatment on the viabilities of H1975 and H460 cells was measured using Cell Counting Kit- 8. Apoptosis was analysed by annexin-V/FITC staining, while protein expressions were assayed by western blotting. Results: Treatment of H1975 and H460 cells with cynaropicrin at doses of 0.25 - 2.0 mu M led to a marked reduction in their viability (p < 0.05). In cynaropicrin-treated H1975 and H460 cells, there was significant increase in apoptosis, when compared to control cells. Caspase-3 and caspase-9 levels were also significantly increased in H1975 and H460 cells on treatment with cynaropicrin at doses of 0.25 and 2.0 mu M while treatment with cynaropicrin at doses of 0.25 - 2.0 mu M significantly down-regulated the mRNA expression of CCND1 in the two cell lines (p < 0.05). Cynaropicrin markedly inhibited mRNA and protein expressions of EGFR, and also downregulated AKT in H1975 and H460 cells (p < 0.05). However, cynaropicrin significantly increased the expressions of miR-202 and miR-370. Conclusion: Cynaropicrin exerts anti-proliferative and proapoptotic effects on H1975 and H460 lung cancer cells via deactivation of EGFR/AKT signaling pathway. Moreover, it upregulated the expressions of miR-202 and miR-370 in these cells. Thus, cynaropicrin has potentials for the treatment of lung cancer.

Automated summary

Cynaropicrin exerts anti-proliferative and proapoptotic effects on H1975 and H460 lung cancer cells by deactivating the EGFR/AKT signaling pathway. It also upregulates the expressions of miR-202 and miR-370 in these cells, indicating its potential for lung cancer treatment.