{"title":"Diagnostic Significance of Beclin-1 and Transforming Growth Factor β in Breast Cancer","authors":"S. Elshaer, L. Rashed, M. A. Hamid","doi":"10.9734/JCTI/2019/V9I130099","DOIUrl":null,"url":null,"abstract":"Background: The main cause of cancer deaths amongst women breast cancer remains a clinical and social challenge, and a serious public health problem. On a worldwide level, it continues to be a devastating disorder.BECN1 is a tumor suppressor gene implicated in the initiation of autophagy. It encodes beclin-1 protein that inhibits cancer growth. There is wide disputation concerning its role in initiation, promotion of tumor and predictive importance of autophagic molecules. Transforming growth factor β (TGF-β) induces process of epithelial-mesenchymal transition (EMT) keeping, epithelial cells more motile and invasive resulting in cancer progression and metastasis. \nAim: Detection of beclin-1 expression level in metastatic and non-metastatic breast cancer patients and study its role in tumorigenesis of breast cancer through attainable association with the inflammatory cytokine, TGF-β. \nMethods: Expression levels of beclin-1 and TGF-β were assessed in 70 breast cancer female patients and 20 controls using quantitative real-time PCR. \nResults: Beclin-1 expression levels as well as TGF-β were significantly higher in metastatic breast cancer patients and non-metastatic patients compared to controls. Positive correlation was found between beclin-1 expression level and TGF-β expression level in breast cancer patients. \nConclusion: Our results indicated that over-expression of both beclin-1 and TGF-β was associated with aggressive clinical outcomes of breast cancer patients and tumor growth. These findings suggest that beclin-1 and TGF-β are associated with tumorigenesis of breast cancer.","PeriodicalId":161223,"journal":{"name":"Journal of Cancer and Tumor International","volume":"39 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2019-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cancer and Tumor International","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.9734/JCTI/2019/V9I130099","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
Background: The main cause of cancer deaths amongst women breast cancer remains a clinical and social challenge, and a serious public health problem. On a worldwide level, it continues to be a devastating disorder.BECN1 is a tumor suppressor gene implicated in the initiation of autophagy. It encodes beclin-1 protein that inhibits cancer growth. There is wide disputation concerning its role in initiation, promotion of tumor and predictive importance of autophagic molecules. Transforming growth factor β (TGF-β) induces process of epithelial-mesenchymal transition (EMT) keeping, epithelial cells more motile and invasive resulting in cancer progression and metastasis.
Aim: Detection of beclin-1 expression level in metastatic and non-metastatic breast cancer patients and study its role in tumorigenesis of breast cancer through attainable association with the inflammatory cytokine, TGF-β.
Methods: Expression levels of beclin-1 and TGF-β were assessed in 70 breast cancer female patients and 20 controls using quantitative real-time PCR.
Results: Beclin-1 expression levels as well as TGF-β were significantly higher in metastatic breast cancer patients and non-metastatic patients compared to controls. Positive correlation was found between beclin-1 expression level and TGF-β expression level in breast cancer patients.
Conclusion: Our results indicated that over-expression of both beclin-1 and TGF-β was associated with aggressive clinical outcomes of breast cancer patients and tumor growth. These findings suggest that beclin-1 and TGF-β are associated with tumorigenesis of breast cancer.