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BackgroundBladder cancer is the most common malignancy in urinary system and the ninth most common malignancy in the world. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression by targeted repression of transcription and translation and play essential roles during cancer development. We investigated the expression of miR-135a in bladder cancer and explored its bio-function during bladder cancer progression.MethodsThe expression of miR-135a in bladder cancer cells and tissues are performed by using Real-time PCR assay. Cell viability assay (MTT assay), colony formation assay, anchorage-independent growth ability assay and Bromodeoxyuridine labeling and immunofluorescence (BrdUrd) assay are used to examine cell proliferative capacity and tumorigenicity. Flow cytometry analysis is used to determine cell cycle progression. The expressions of p21, p27, CyclinD1, Ki67, PHLPP2 and FOXO1 are measured by Western blotting assay. Luciferase assay is used to confirm whether FOXO1 is the direct target of miR-135a.ResultsmiR-135a is upregulated in bladder cancer cells and tissues. Enforced expression of miR-135a promotes bladder cancer cells proliferation, whereas inhibition of miR-135a reverses the function. Furthermore, for the first time we demonstrated PHLPP2 and FOXO1 are direct targets of miR-135a and transcriptionally down-regulated by miR-135a. Suppression of PHLPP2 or FOXO1 by miR-135a, consisted with dysregulation of p21, p27, Cyclin D1 and Ki67, play important roles in bladder cancer progression.ConclusionOur study demonstrates that miR-135a promotes cell proliferation in bladder cancer by targeting PHLPP2 and FOXO1, and is performed as an onco-miR.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-015-0438-8) contains supplementary material, which is available to authorized users.

Rationale and Objectives The purpose of this study was to determine textural features that show a significant difference between carcinomatous tissue and the bladder wall on magnetic resonance imaging (MRI) and explore the feasibility of using them to differentiate malignancy from the normal bladder wall as an initial step for establishing MRI as a screening modality for the noninvasive diagnosis of bladder cancer. Materials and Methods Regions of interest (ROIs) were manually placed on foci of bladder cancer and uninvolved bladder wall in 22 patients and on the normal bladder wall of 23 volunteers to calculate 40 known textural features. Statistical analysis was applied to determine the difference in these features in bladder cancer versus uninvolved bladder wall versus normal bladder wall of volunteers. The significantly different features were then analyzed using a support vector machine (SVM) classifier to determine their accuracy in differentiating malignancy from the bladder wall. Results Thirty-three of 40 features show significant differences between bladder cancer and the bladder wall. Nine of 40 features were significantly different in uninvolved bladder wall of patients versus normal bladder wall of volunteers. Further study indicates that seven of these 33 features were significantly different between uninvolved bladder wall of patients with early cancer and that of volunteers, whereas 15 of 33 features were different between that of patients with advanced cancer and normal wall. With the testing dataset consisting of ROIs acquired from patients, the classification accuracy using 33 textural features fed into the SVM classifier was 86.97%. Conclusion The initial experience demonstrates that texture features are sensitive to reveal the differences between bladder cancer and the bladder wall on MRI. The different features can be used to develop a computer-aided system for the evaluation of the entire bladder wall.

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Pirfenidone (esbiret) is an established anti-fibrotic and anti-inflammatory drug used to treat idiopathic pulmonary fibrosis. In the present study, the dose-dependent effects of pirfenidone on the cell cycle, proliferation and expression of heat shock protein (HSP)-47 and collagen type I in a cultured rat hepatic stellate cell line (HSC-T6) were investigated. Following pirfenidone treatment, cell proliferation was determined using the cell counting kit-8 assay and the cell cycle was measured using flow cytometry. HSP-47 expression was estimated using western blot analysis and collagen type I mRNA was assessed using reverse transcription quantitative polymerase chain reaction. Pirfenidone induced significant dose-dependent inhibition of proliferation in HSC-T6 cells. Cell viability was unaffected by treatment with pirfenidone (0, 10 or 100 µM) for 24 and 72 h. However, after 24 h, HSC-T6 cells exhibited dose-dependent decreases in HSP-47 protein and collagen I mRNA levels. In conclusion, pirfenidone inhibited HSC-T6 cell proliferation, arrested the cell cycle and reduced the expression of HSP-47 and collagen type I, indicating that pirfenidone may be a promising drug in the treatment of liver fibrosis.

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