{"title":"Mucoxin (Acetogenin) Inhibits Proliferation of T47D Breast Cancer by Suppressing Expression of Cyclin D1 Mediated by p53","authors":"Muhartono Muhartono, Sutyarso Sutyarso, M. Kanedi","doi":"10.3923/IJCR.2016.101.108","DOIUrl":null,"url":null,"abstract":"Background: Mucoxinis believed to be a promising anticancer because it is known to inhibit cell proliferation. However, given study on \nmucoxin still very limited, the mechanism of the substances isolated from leaf extract of \nRollinia mucosa in regulating and eliminating \ncancer cells has not fully understood. This study investigated the mucoxin mechanism in affecting proliferation, expression of p53 and \ncyclin D1 genes in the T47D breast cancer cells. Materials and Methods: The cell line samples were grouped into four referred to the hour \nof assays undertaken after mucoxin application, namely hour 0th, 24th, 48th and 72nd. Each group was given mucoxin of six different \nconcentrations namely 0.00 µg mLG \n1 \n as a control, 0.1×10G \n3 \n, 0.5×10G \n3 \n, 1×10G \n3 \n, 5×10G \n3 \n and 10×10 \nS3 \n µg mLG \n with three replications. \nCells proliferation assayed by flow cytometry technique using BrDU staining protocol, whereas the expression of p53 and cyclin D1 genes \ndetermined by quantitative PCR (qPCR). Results: Cell proliferation in each group significantly reduced by mucoxin treatment. \n and \n10×10 \nMucoxin enhance p53 gene expression in 48 h, while the expression of cyclin D1 supressed signifantly by mucoxin of 5×10G \nS3 \n µ g mL G \n in 48 and 72 h. Simple regression analysis showed that cell proliferation decreased with the increase of p53 expression \nand the suppression of cyclin D1 gene, while p53 expression positively associated to cyclin D1 expression. Conclusion: Mucoxin can \n1 \ndecrease the proliferation of T47D breast cancer cells by suppressing the expression of cyclin D1 mediated by p53 gene.","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"12 2 1","pages":"101-108"},"PeriodicalIF":0.0000,"publicationDate":"2016-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of cancer research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3923/IJCR.2016.101.108","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
Background: Mucoxinis believed to be a promising anticancer because it is known to inhibit cell proliferation. However, given study on
mucoxin still very limited, the mechanism of the substances isolated from leaf extract of
Rollinia mucosa in regulating and eliminating
cancer cells has not fully understood. This study investigated the mucoxin mechanism in affecting proliferation, expression of p53 and
cyclin D1 genes in the T47D breast cancer cells. Materials and Methods: The cell line samples were grouped into four referred to the hour
of assays undertaken after mucoxin application, namely hour 0th, 24th, 48th and 72nd. Each group was given mucoxin of six different
concentrations namely 0.00 µg mLG
1
as a control, 0.1×10G
3
, 0.5×10G
3
, 1×10G
3
, 5×10G
3
and 10×10
S3
µg mLG
with three replications.
Cells proliferation assayed by flow cytometry technique using BrDU staining protocol, whereas the expression of p53 and cyclin D1 genes
determined by quantitative PCR (qPCR). Results: Cell proliferation in each group significantly reduced by mucoxin treatment.
and
10×10
Mucoxin enhance p53 gene expression in 48 h, while the expression of cyclin D1 supressed signifantly by mucoxin of 5×10G
S3
µ g mL G
in 48 and 72 h. Simple regression analysis showed that cell proliferation decreased with the increase of p53 expression
and the suppression of cyclin D1 gene, while p53 expression positively associated to cyclin D1 expression. Conclusion: Mucoxin can
1
decrease the proliferation of T47D breast cancer cells by suppressing the expression of cyclin D1 mediated by p53 gene.