Momordica cochinchinensis (Gac) Aril Suppresses Proliferation and Induces Apoptosis of Colorectal Cancer Cells

Document Type : Research Articles


1 Department of Pathology, School of Medicine, University of Phayao, Thailand.

2 Unit of Excellence of Pharmacological Research on Medicinal Plants, University of Phayao, Thailand.

3 Division of Pharmacology, Department of Pharmaceutical Care, School of Pharmaceutical Sciences, University of Phayao, Thailand.

4 Department of Pharmaceutical Care, School of Pharmaceutical Sciences, University of Phayao, Thailand.

5 Department of Microbiology, School of Medical Science, University of Phayao, Thailand.


Background: Gac aril contains high level of carotenoids. This carotenoid possesses several pharmacological properties including antioxidant, anti-inflammatory, and anti-tumor activities. Objective: To investigate the anti-cancer activity of Gac aril extract on human colorectal cancer cells and its related mechanisms. Methods: Colorectal cancer cell lines HCT116 and HT29 were treated with Gac aril extract and its effects on cytotoxicity and anti-proliferation were analyzed using the MTT/MTS and colony formation assay, respectively. Then, further related mechanisms responsible for anti-proliferation were investigated by cell death detection ELISA and Flow cytometry. Results: The results showed that treated cells became rounded up and there was a loss of contact with neighboring cells, leading to a reduction of cell viability. The cytotoxic effects were evaluated IC50 for HCT116 and HT29 cells were 2.16 mg/mL and 1.29 mg/mL, respectively but it not toxic to normal HEK293 at the same dose. Moreover, Gac aril extract significantly inhibits proliferative ability with increasing concentrations having a greater effect. Subsequently, the cellular mechanism responsible for suppressive proliferation was validated. It shows apoptosis induction and arrest of cell cycle. Conclusion: Our findings demonstrated that Gac aril extract can induce apoptosis and arrest of cell cycle at S and G2/M phases in both HCT116 and HT29 colorectal cancer cells. 


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