The “good-cop bad-cop” TGF-beta role in breast cancer modulated by non-coding RNAs

Publication date: Available online 11 April 2017
Source:Biochimica et Biophysica Acta (BBA) - General Subjects
Author(s): Gulei Diana, Nikolay Mehterev, Hui Ling, Giorgio Stanta, Braicu Cornelia, Berindan-Neagoe Ioana
BackgroundLack of early diagnosis methods and the development of drug resistance are among the main reasons for increased mortality rates within breast cancer patients. These two aspects are governed by specific pro-carcinogenic modifications, where TGBß-induced EMT is one of the leading actors. Endowment of the epithelial cells with mesenchymal characteristics allows them to migrate and invade secondary tissues in order to form malignant sites and also confers chemoresistance. TGFß which role switches from the tumor suppressor cytokine to the oncogenic one favoring the tumor microenvironment regulates this process.Scope of ReviewThis review aims to comprehensively present the updated TGFß-induced EMT in breast cancer, including the regulatory role of the non-codingRNAs with focus on the miR-200 family and newly discovered lncRNAs such as HOTAIRM1. Additionally, a new phenotype, P-EMT, also modulated by miR-200 and miR-34 families that form complex feedback loops with TGFß, SNAI1 and ZEB1/2 is presented under an updated form.Major conclusionsThe hallmarks of EMT are becoming increasingly associated with aggressive forms of breast cancer and low survival rates among patients. Considering that this phenotypical switch can trigger drug resistance, invasion and metastasis, inhibition of EMT could represent an important milestone in mammary cancer treatment.General significanceThe present review assembles the most recent data regarding TGFß induced EMT, including the input of non-coding RNAs, contributing to the possible development of new targeted treatment strategies for cancer patients.



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