Kanthanadon DittharotSumana DakengParichat SuebsakwongApichart SuksamrarnPimpicha PatmasiriwatMoltira PromkanRamkhamhaeng UniversityFaculty of Medicine, Ramathibodi Hospital, Mahidol UniversityMahidol University2020-01-272020-01-272019-01-01Planta Medica. Vol.85, No.5 (2019), 370-37814390221003209432-s2.0-85062943467https://repository.li.mahidol.ac.th/handle/20.500.14594/50369© 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.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyChemistryMedicineArticleSCOPUS10.1055/a-0791-1591