Publication: Cucurbitacin B Induces Hypermethylation of Oncogenes in Breast Cancer Cells
Issued Date
2019-01-01
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ISSN
14390221
00320943
00320943
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2-s2.0-85062943467
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Mahidol University
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SCOPUS
Bibliographic Citation
Planta Medica. Vol.85, No.5 (2019), 370-378
Suggested Citation
Kanthanadon Dittharot, Sumana Dakeng, Parichat Suebsakwong, Apichart Suksamrarn, Pimpicha Patmasiriwat, Moltira Promkan Cucurbitacin B Induces Hypermethylation of Oncogenes in Breast Cancer Cells. Planta Medica. Vol.85, No.5 (2019), 370-378. doi:10.1055/a-0791-1591 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/50369
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Title
Cucurbitacin B Induces Hypermethylation of Oncogenes in Breast Cancer Cells
Abstract
© Georg Thieme Verlag KG Stuttgart. New York. Breast cancer is a complex disease driven by multiple factors including both genetic and epigenetic alterations. Recent studies revealed that abnormal gene expression induced by epigenetic changes including aberrant promoter methylation plays a critical role in human breast carcinogenesis. Cucurbitacin B has antiproliferative activity against various human breast cancer cells, but the molecular mechanism is not completely understood. In this study, we explore the influence of cucurbitacin B from Trichosanthes cucumerina on the methylation status at the promoter of oncogenes c-Myc, cyclin D1, and survivin in breast cancer cell lines. Growth inhibitory effect of cucurbitacin B on breast cancer cells was assessed by MTT assay and colony formation assay. Methylation status of genomic DNA was determined by methylation-specific PCR. Gene and protein expression levels of all genes studied were analyzed by real-time RT-PCR and western blot. The results indicated that cucurbitacin B could inhibit cell growth in breast cancer cells. The oncogene promoters are usually hypomethylated in cancer cells. Upon cucurbitacin B treatment, upregulation of DNMT1 and obvious heavy methylation in the promoters of c-Myc, cyclin D1, and survivin, which consequently downregulated the expression of all these oncogenes, were observed. Hence, cucurbitacin B proved to be a potential cancer therapeutic agent, in part by inducing hypermethylation and silences the oncogenic activation.