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Transglutaminase 2: The Maestro of the Oncogenic Mediators in Renal Cell Carcinoma

Department of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Kayisdagi Cad., Istanbul 34755, Turkey
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Med. Sci. 2019, 7(2), 24; https://doi.org/10.3390/medsci7020024
Received: 26 November 2018 / Revised: 1 February 2019 / Accepted: 1 February 2019 / Published: 6 February 2019
(This article belongs to the Special Issue Transglutaminases in Health and Disease)
Transglutaminase 2 (TG2) is a multifunctional crosslinking enzyme that displays transamidation, protein disulfide isomerase, protein kinase, as well as GTPase and ATPase activities. TG2 can also act as an adhesion molecule involved in the syndecan and integrin receptor signaling. In recent years, TG2 was implicated in cancer progression, survival, invasion, migration, and stemness of many cancer types, including renal cell carcinoma (RCC). Von Hippel-Lindau mutations leading to the subsequent activation of Hypoxia Inducible Factor (HIF)-1-mediated signaling pathways, survival signaling via the PI3K/Akt pathway resulting in Epithelial Mesenchymal Transition (EMT) metastasis and angiogenesis are the main factors in RCC progression. A number of studies have shown that TG2 was important in HIF-1- and PI3K-mediated signaling, VHL and p53 stabilization, glycolytic metabolism and migratory phenotype in RCC. This review focuses on the role of TG2 in the regulation of molecular pathways nurturing not only the development and propagation of RCC, but also drug-resistance and metastatic potential. View Full-Text
Keywords: Transglutaminase 2 (TG2); Renal Cell Carcinoma (RCC); metastasis; invasion; epithelial mesenchymal transition Transglutaminase 2 (TG2); Renal Cell Carcinoma (RCC); metastasis; invasion; epithelial mesenchymal transition
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Nezir, A.E.; Ulukan, B.; Telci, D. Transglutaminase 2: The Maestro of the Oncogenic Mediators in Renal Cell Carcinoma. Med. Sci. 2019, 7, 24.

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