Camelliol C inhibits viability, migration, and invasion of human cervical cancer cells via induction of apoptosis, G2/M cell cycle arrest, and blocking of PI3K/AKT signalling pathway

山茶酚C通过诱导细胞凋亡、G2/M期细胞周期阻滞和阻断PI3K/AKT信号通路,抑制人宫颈癌细胞的活力、迁移和侵袭。

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Abstract

INTRODUCTION: Cervical cancer is a devastating cancer and is currently ranked as the fourth most prevalent type of cancer in the world. The lack of efficacious chemotherapy forms a bottleneck in the treatment of cervical cancer. This study was therefore undertaken to evaluate the anticancer effects of camelliol C against human cervical cancer cells. MATERIAL AND METHODS: Normal cell line (NCEC) and cervical cancer cell lines (Csdki, HeLa, C33A, and siHa) were used in this study. Cell viability was determined by MTT assay, and apoptosis was detected by DAPI and annexin V/PI staining. Cell cycle analysis, ROS, and MMP levels were examined by flow cytometry. Cell migration and invasion was monitored by transwell assays. RESULTS: The results showed that camelliol C inhibits the proliferation of all the human cervical cancer cell lines with IC(50) ranging from 10 to 20 µM. However, comparatively low antiproliferative effects were observed on the normal cells. Investigation of the underlying mechanisms showed that camelliol C induces apoptosis in HeLa cancer cells. Camelliol C-triggered apoptosis was also linked with cleavage of caspase-3 and -9, and PARP. Additionally, the Bax protein levels were increased and those of Bcl-2 were decreased. Transwell assays showed that camelliol C suppresses the migration and invasion of the HeLa cervical cancer cells. Additionally, camelliol C also blocked the PI3K/AT signalling cascade dose dependently. CONCLUSIONS: Camelliol C may prove beneficial in the treatment of cervical cancer.

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