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These data suggest that the HDACi-elicited upregulation of TRPM2 expression is required for HDACi-induced apoptosis in bladder cancer cells and that HDACi activated the enrichment of H3K9Ac-represented permissive chromatin in TRPM2 promoter.

Bladder outlet obstruction is a common disease, which always evokes urinary bladder wall remodeling significantly. It has been suggested that bladder outlet obstruction can make the bladder progression from inflammation to fibrosis, and hypoxia may play a vital role. It has been found the expression of microRNA‐101 varied in bladder after BOO. But what role microRNA‐101 and hypoxia play in bladder is not well known. This study is to investigate the mechanism of microRNA‐101 and hypoxia in fibrosis of bladder after BOO. We found the expression of microRNA‐101 and hif‐1α increased in bladder after BOO. Hypoxia could promote the expression of extracellular matrix subtypes and microRNA‐101 in BSMCs. When microRNA‐101b was translated into BSMCs, the smad2/3 signaling pathway was found to repress. Dual luciferase reporter detected that microRNA‐101b attenuated the TGF‐β signaling pathway by inhibiting the expression of TGFβR1. Then, we conclude microRNA‐101b is induced by hypoxia and represses fibrosis of BSMCs by inhibiting the expression of TGFβR1 through TGF‐β signaling pathway, and it may be an anti‐fibrotic miRNA for therapy. © 2018 IUBMB Life, 71(1):235–243, 2019

E2 is significantly associated with prostate volume. High concentrations of E2 may be a risk factor for the large volume of prostate.

Taken together, the present study revealed a set of critical genes, which can provide etiologic clues as to enzalutamide-resistant prostate cancer and guide novel therapeutic approaches.

Objective AT-rich interactive domain-containing protein 1A (ARID1A) is frequently mutated or deficient in various types of tumors. However, the role of ARID1A in bladder cancer remains unclear. We aimed to evaluate ARID1A expression and its biological role and correlation with prognosis in patients with urothelial bladder carcinoma (BUC). Methods ARID1A expression levels in BUC and normal tissues were assessed by immunohistochemistry and correlated with clinicopathological characteristics and patient outcomes. Downregulation of ARID1A was mimicked by transfection with small interfering RNA in T24 bladder cancer cells, and the effects on cell proliferation and migration were evaluated. Results ARID1A expression was significantly reduced in BUC tissues and was significantly associated with T stage and AJCC stage. Upregulation of ARID1A predicted a better prognosis in BUC patients. ARID1A expression and lymph node status were identified as independent prognostic factors for overall survival. Silencing of ARID1A promoted the proliferation of BUC cells. Conclusions ARID1A may represent a novel diagnostic and prognostic biomarker in patients with BUC.

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