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Abstract Title:

Cucurbitacin B Induces Hypermethylation of Oncogenes in Breast Cancer Cells.

Abstract Source:

Planta Med. 2019 Mar ;85(5):370-378. Epub 2018 Nov 21. PMID: 30463098

Abstract Author(s):

Kanthanadon Dittharot, Sumana Dakeng, Parichat Suebsakwong, Apichart Suksamrarn, Pimpicha Patmasiriwat, Moltira Promkan

Article Affiliation:

Kanthanadon Dittharot

Abstract:

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 fromon 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.

Study Type : In Vitro Study

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Sayer Ji
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