Abstract
The regulatory role of coptisine on autophagy in cervical cancer cells (in HcerEpic, HeLa, and SiHa) was examined by assessment of cell viability, colony formation, and apoptosis. Coptisine, in a dose-dependent fashion, significantly inhibited cervical cancer cell viability as measured by cell proliferation, transwell, and TUNEL assays. Coptisine inhibited the levels of p62 and Bcl-2, whilst it promoted the accumulation of Atg5, LC3Ⅱ/LC3Ⅰ and Bax. These data taken together suggest that coptisine inhibits the progression of cervical cancer cells by enhancing autophagy through suppression of the PI3K/AKT/mTOR pathway. This represents a theoretical foundation for developing novel cervical cancer treatments.
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