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Cucurbitacin B Induces Hypermethylation of Oncogenes in Breast Cancer Cells.
Dittharot, Kanthanadon; Dakeng, Sumana; Suebsakwong, Parichat; Suksamrarn, Apichart; Patmasiriwat, Pimpicha; Promkan, Moltira.
Afiliação
  • Dittharot K; Office of Research Academic and Innovation, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
  • Dakeng S; Department of Clinical Microscopy, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, Thailand.
  • Suebsakwong P; Department of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Ramkhamhaeng University, Bangkok, Thailand.
  • Suksamrarn A; Department of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Ramkhamhaeng University, Bangkok, Thailand.
  • Patmasiriwat P; Department of Clinical Microscopy, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, Thailand.
  • Promkan M; Department of Clinical Microscopy, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, Thailand.
Planta Med ; 85(5): 370-378, 2019 Mar.
Article em En | MEDLINE | ID: mdl-30463098
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.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Triterpenos / Neoplasias da Mama / Regulação Neoplásica da Expressão Gênica / Trichosanthes / Antineoplásicos Fitogênicos Limite: Female / Humans Idioma: En Revista: Planta Med Ano de publicação: 2019 Tipo de documento: Article País de afiliação: Tailândia

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Triterpenos / Neoplasias da Mama / Regulação Neoplásica da Expressão Gênica / Trichosanthes / Antineoplásicos Fitogênicos Limite: Female / Humans Idioma: En Revista: Planta Med Ano de publicação: 2019 Tipo de documento: Article País de afiliação: Tailândia