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Year : 2015  |  Volume : 11  |  Issue : 44  |  Page : 237-243

Poncirus trifoliata Rafin. induces the apoptosis of triple-negative breast cancer cells via activation of the c-Jun NH(2)-terminal kinase and extracellular signal-regulated kinase pathways

1 Department of Oral Pathology, School of Dentistry, Institute of translational Dental Sciences, Yangsan, South Korea
2 Division of Pharmacology, School of Korean Medicine, Pusan National University, Yangsan, South Korea
3 Department of Herbology, College of Korean Medicine, Wonkwang University, Iksan, South Korea
4 Department of Preventive and Community Dentistry, School of Dentistry, Pusan National University, Yangsan, South Korea

Correspondence Address:
Hyungwoo Kim
School of Korean Medicine, Pusan National University, Yangsan City, Gyeongnam, 626-870
South Korea
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Source of Support: Supported by a grant of the Korean Health Technology R and D Project, Ministry of Health and Welfare, Republic of Korea (A101420), Conflict of Interest: None

DOI: 10.4103/0973-1296.166056

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Background: Poncirus trifoliataRafin. is a traditional medicine with known anti-inflammatory and anti-cancer properties. Traditionally, it is used to control chronic inflammation, allergy and gastrointestinal diseases such as digestive ulcers gastritis in China, Japan, and Korea. Objectives: To evaluate the apoptosis-inducing activity of a P. trifoliatamethanol extract (MEPT) and elucidate the molecular mechanisms. Materials and Methods: The anti-cancer effect of MEPT and its underlying mechanisms were investigated in breast cancer cells using 3,4,5-dimethyl N-methylthiazol-2-yl-2, 5-d-phenyl tetrazolium bromide assay, cell cycle analysis, and western blotting. Results: MEPT suppressed the proliferation of MDA-MB-231 cells with inhibition dose 50% value of 119.44 μg/mL at 24 h, which have features typical of triple-negative breast cancer cells. MEPT also altered the characteristic features of the MDA-MB-231 cells and increased the proportion of cells undergoing sub-G1 arrest. In addition, MEPT increased levels of caspase 8 and 3 in MDA-MB-231 cells, whereas caspase 9 was not detected. In addition, MEPT-induced tumor necrosis factor receptor (TNFR) and TNFR type 1-associated death domain (TRADD) protein and the activations of c-Jun NH(2)-terminal kinase (JNK) and extracellular signal-regulated kinases (ERK). Conclusion: Our results indicate that MEPT has chemotherapeutic potential in triple-negative breast cancer and that at the molecular level its effects are derived from the activations of TNFR and of the mitogen-activated protein kinase pathway.

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