Irma Yanti Rangkuti, P. Hasibuan, T. Widyawati, Y. Siregar
{"title":"Metformin Inhibits Growth of Breast Cancer Cell T47 through Decreasing Expression of Protein P53, BCL2 and Cyclin D1","authors":"Irma Yanti Rangkuti, P. Hasibuan, T. Widyawati, Y. Siregar","doi":"10.32892/JMRI.164","DOIUrl":null,"url":null,"abstract":"Breast cancer is a disease that afflicts women only 0.5 to 1 % are male breast cancers.Breast cancer has several variants and requires a different therapeutic approach, and until now the therapy has not been satisfactory due to the emergence of resistance. Metformin as the main choice drug type 2 diabetes mellitus which is known to have a cytotoxic effect for breast cancer. This study aimed to analyze metformin cytotoxic mechanisms covering the cell cycle , apoptosis, expression of p53, bcl-2 and cyclin D1 T47D cells which exposed to metformin HCl. The study was conducted invitro on T47D breast cancer cells which exposed to metformin concentrations of 1738.2 µg / mL and 3476.4 µg / mL and doxorubicin concentrations of 0.1µg / mL and 0.2µg / mL for 24 hours. Cell cycle testing and apoptosis using the flowsitometry method and expression test of p53 protein, bcl-2 dancycline D1 in T47D cells with immunocytochemistry. Data was analyzed by one way Anova with Bonferroni's advanced test. The results showed that metformin inhibited the G0-G1 phase of the T47D cell cycle, triggered T47D cell apoptosis, significantly reduced p53, bcl-2 and cyclin D1 protein expression (p <0.05). Conclusion of the study, metformin inhibits T47D cells through inhibition of the cell cycle G0-G1 phase, reducing protein expression p53, bcl-2 and cyclin D1.","PeriodicalId":73819,"journal":{"name":"Journal of medical research and innovation","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of medical research and innovation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.32892/JMRI.164","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Breast cancer is a disease that afflicts women only 0.5 to 1 % are male breast cancers.Breast cancer has several variants and requires a different therapeutic approach, and until now the therapy has not been satisfactory due to the emergence of resistance. Metformin as the main choice drug type 2 diabetes mellitus which is known to have a cytotoxic effect for breast cancer. This study aimed to analyze metformin cytotoxic mechanisms covering the cell cycle , apoptosis, expression of p53, bcl-2 and cyclin D1 T47D cells which exposed to metformin HCl. The study was conducted invitro on T47D breast cancer cells which exposed to metformin concentrations of 1738.2 µg / mL and 3476.4 µg / mL and doxorubicin concentrations of 0.1µg / mL and 0.2µg / mL for 24 hours. Cell cycle testing and apoptosis using the flowsitometry method and expression test of p53 protein, bcl-2 dancycline D1 in T47D cells with immunocytochemistry. Data was analyzed by one way Anova with Bonferroni's advanced test. The results showed that metformin inhibited the G0-G1 phase of the T47D cell cycle, triggered T47D cell apoptosis, significantly reduced p53, bcl-2 and cyclin D1 protein expression (p <0.05). Conclusion of the study, metformin inhibits T47D cells through inhibition of the cell cycle G0-G1 phase, reducing protein expression p53, bcl-2 and cyclin D1.