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International Journal of Pharmacology

Year: 2021 | Volume: 17 | Issue: 5 | Page No.: 339-349
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Benjaporn Buranrat

Benjaporn Buranrat

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Research Article

Growth Inhibition, Apoptosis Induction and Migratory Suppression by Careya arborea Leaf Extract in HeLa Cervical Cells

Benjaporn Buranrat Benjaporn Buranrat's LiveDNA
Background and Objective: Careya arborea (CA) is a plant or vegetable found in Thailand and consumed as a fresh vegetable that reported anticancer effect. The action of CA on growth, apoptosis and migration of cervical HeLa cancer cells and underlying mechanism has not been explored. So, current article studied the human HeLa cervical cancer cell to examine the anticancer action of DW and ethanolic CA extract. Materials and Methods: HeLa cell was treated with the different doses of CA extract (DW and 95% ethanol) and the viability was determined by SRB and cell cycle distribution method. Apoptosis was determined by AO/EB staining, Annexin V-FITC and PI staining, ROS production. Cells migration was examined by wound healing method. Results: Treatment with both of CA extracts promoted HeLa cell death correlating with suppression the colony formation by dose-dependent manner. The ethanolic extract had more potency than DW extract with lower IC50 values of SRB and colony formation assay. CA extracts significantly inhibited the cancer cell distribution at G0/G1 phase and stimulated apoptosis after detecting with AO/EB staining and confirming with flow cytometry. Increased late apoptotic cell death was indicated after incubating with CA extract and the percentage were 66.2% for DW extract and 35% for ethanolic extract. The mechanism of CA extract on cell death and apoptosis were detected about reduction of mitochondrial function and induction of ROS formation. Lastly, CA suppressed the cancer cells migration in a concentration-dependent manner, especially high CA dose. Conclusion: Treatment with CA extract tends to increase death, stimulate of apoptosis and reduce migration capability of cervical cancer cells through increasing ROS formation and attenuating mitochondrial function.
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