Epithelial to Mesenchymal Transition in Renal Cell Carcinoma: Implications for Cancer Therapy
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REVIEW ARTICLE
Epithelial to Mesenchymal Transition in Renal Cell Carcinoma: Implications for Cancer Therapy Francesco Piva1 • Matteo Giulietti1 • Matteo Santoni2 • Giulia Occhipinti1 • Marina Scarpelli3 • Antonio Lopez-Beltran4 • Liang Cheng5 • Giovanni Principato1 Rodolfo Montironi3
•
Ó Springer International Publishing Switzerland 2016
Abstract Epithelial-to-mesenchymal transition (EMT) is a developmentally vital reversible process by which fully differentiated cells lose their epithelial features and acquire a migratory mesenchymal phenotype. EMT contributes to the metastatic potential of tumors. The expression profile and other biological properties of EMT suggest potential targets for cancer therapy, including in renal-cell carcinoma (RCC). The preclinical and clinical results have substantiated the promises that dysregulated elements leading to EMT can be a potential target in RCC patients. In this study, we illustrated the pathogenic and prognostic role of EMT in RCC. In addition, we reconstructed, by literature analysis, the different pathways implicated in the EMT process, thus supporting the rational for future EMTdirected therapeutic approaches for RCC patients.
Key points Epithelial-to-mesenchymal transition (EMT) is a reversible process which leads to the loss of epithelial features and to the acquisition of a mesenchymal phenotype. EMT plays a crucial role in RCC development and progression. Targeting EMT components seems to represent an attractive therapeutic strategy in RCC patients.
1 Introduction
& Francesco Piva [email protected] 1
Department of Specialistic Clinical and Odontostomatological Sciences, Polytechnic University of Marche Region, 60131 Ancona, Italy
2
Clinica di Oncologia Medica, AOU Ospedali Riuniti, Universita` Politecnica delle Marche, via Conca 71, 60126 Ancona, Italy
3
Section of Pathological Anatomy, Polytechnic University of the Marche Region, School of Medicine, United Hospitals, Ancona, Italy
4
Department of Pathology and Surgery, Faculty of Medicine, University of Cordoba, Cordoba, Spain
5
Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA
Renal-cell carcinoma (RCC) is the most common tumor of the kidney, clear-cell RCC (ccRCC) being the most frequent histological subtype. RCC is an immunogenic tumor and is characterized by chemo- and radio-resistance. Approximately 30 % of RCC tumors are already metastatic at initial diagnosis, with other 30–40 % of patients who develop distant metastases after initial nephrectomy [1]. Metastatic RCC dissemination is often initiated by reactivating an embryonic development program, such as the epithelial-to-mesenchymal-transition (EMT) [2]. Through the EMT process, fully differentiated cells lose their cell polarity and cell–cell adhesion features and gain a migratory and invasive mesenchymal phenotype. Loss of E-cadherin is considered to be a crucial event in EMT. This is the result of the increased expression of transcriptional repressors of E-cadherin expression,
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