Abstract
Bladder cancer is one of the most incident neoplasms worldwide, and its treatment remains a significant challenge, since the mechanisms underlying disease progression are still poorly understood. The epithelial to mesenchymal transition (EMT) has been proven to play an important role in the tumorigenic process, particularly in cancer cell invasiveness and metastatic potential. Several studies have reported the importance of epigenetic mechanisms and enzymes, which orchestrate them in several features of cancer cells and, specifically, in EMT. In this paper, we discuss the epigenetic enzymes, protein-coding and non-coding genes, and mechanisms altered in the EMT process occurring in bladder cancer cells, as well as its implications, which allows for improved understanding of bladder cancer biology and for the development of novel targeted therapies.
Highlights
Kottakis et al suggested that enhancer of zeste homolog 2 (EZH2) might be regulated by FGF-2 upregulation in Bladder CancerBladder cancer (BlCa) cells, which, in turn, upregulates the lysine demethylase 2B (KDM2B) and triggers EZH2 recruitment
Serine protease PRSS8 was found to be downregulated by promoter methylation in high-grade BlCa tissues, and its overexpression in cell lines was associated with E-Cadherin upregulation, which suggests an interplay between these two proteins during epithelial differentiation [42,43]
Martínez-Fernández et al [74] showed that PRC members EZH2 and BMI1 repress miR200 family, which results in epithelial to mesenchymal transition (EMT) activation and aggressive disease, which is in accordance with the association of EZH2 overexpression with high risk for recurrence in NMIBC [114]
Summary
Bladder cancer (BlCa) is the seventh most prevalent cancer worldwide and the second most frequent urological malignancy after prostate cancer. Incidence has been rising in most countries, with an estimated 549,393 new cases diagnosed in 2018 and 990,724 new cases expected in 2040. Similar to other urological malignancies, mortality-to-incidence ratios are higher in underdeveloped countries, which probably reflects different environmental exposures and/or inequalities in healthcare accessibility [4]. Non-muscle invasive BlCa (NMIBC, corresponding to 75% to 80% of all cases, disclosing papillary architecture, with the propensity to recur and eventually invade the bladder wall over time) and muscle-invasive BlCa (MIBC, 20% to 25% of all cases, mostly derived from urothelial carcinoma in situ, which constitutes an aggressive disease that invades locally and metastasizes systemically) [6,7]
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