Mohammad Abbasi-Kolli, Shirin Shahbazi, Loabat Geranpayeh
{"title":"Down-regulation of <i>RB1</i> and miR-132 in ductal carcinoma of the breast.","authors":"Mohammad Abbasi-Kolli, Shirin Shahbazi, Loabat Geranpayeh","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>miR-132-3p acts in normal breast development and its downregulation has been documented in breast cancer. One of the targets of miR-132-3p is <i>RB1</i> which is also inactivated in breast cancer. The interactions between <i>RB1</i> and miR-132 have been reported in several pathological conditions. We aimed to investigate the correlation between expression levels of miR-132 and <i>RB1</i> in ductal carcinoma of the breast.</p><p><strong>Methods: </strong>The study was carried out on tissues obtained from female patients with primary breast cancer. Tumor samples were classified using clinical and pathological data. Following RNA extraction and cDNA synthesis, relative gene expressions in tumors were compared to non-cancerous adjacent tissues. The link between <i>RB1</i> and miR-132 was assessed by the correlation coefficient test.</p><p><strong>Results: </strong>Our findings revealed a significant decrease in miR-132 and <i>RB1</i> expressions with a ratio of 0.165 and 0.365, respectively. Tumor grade showed an association with miRNA-132 levels. The expression of miR-132 in grade I tumors was almost equal to that of normal adjacent tissues, but was intensely decreased in grades II and III. The correlation analysis showed a small linear association between <i>RB1</i> and miR-132 levels.</p><p><strong>Conclusion: </strong>The reduction of miR-132 and <i>RB1</i> expression confirmed the tumor-suppressive role of both genes in breast cancer. Considering that <i>RB1</i> is one of the miR-132 targets, further studies are required to discover any miRNA-mediated upregulation role for miR-132. Our finding discovered a small linear association between miR-132 and <i>RB1</i>, which can be concluded towards their independent function in breast cancer pathogenesis.</p>","PeriodicalId":73460,"journal":{"name":"International journal of molecular epidemiology and genetics","volume":"14 1","pages":"1-10"},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10195390/pdf/ijmeg0014-0001.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of molecular epidemiology and genetics","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: miR-132-3p acts in normal breast development and its downregulation has been documented in breast cancer. One of the targets of miR-132-3p is RB1 which is also inactivated in breast cancer. The interactions between RB1 and miR-132 have been reported in several pathological conditions. We aimed to investigate the correlation between expression levels of miR-132 and RB1 in ductal carcinoma of the breast.
Methods: The study was carried out on tissues obtained from female patients with primary breast cancer. Tumor samples were classified using clinical and pathological data. Following RNA extraction and cDNA synthesis, relative gene expressions in tumors were compared to non-cancerous adjacent tissues. The link between RB1 and miR-132 was assessed by the correlation coefficient test.
Results: Our findings revealed a significant decrease in miR-132 and RB1 expressions with a ratio of 0.165 and 0.365, respectively. Tumor grade showed an association with miRNA-132 levels. The expression of miR-132 in grade I tumors was almost equal to that of normal adjacent tissues, but was intensely decreased in grades II and III. The correlation analysis showed a small linear association between RB1 and miR-132 levels.
Conclusion: The reduction of miR-132 and RB1 expression confirmed the tumor-suppressive role of both genes in breast cancer. Considering that RB1 is one of the miR-132 targets, further studies are required to discover any miRNA-mediated upregulation role for miR-132. Our finding discovered a small linear association between miR-132 and RB1, which can be concluded towards their independent function in breast cancer pathogenesis.