Background Circular RNAs (circRNAs) have been considered to mediate occurrence and development of human cancers, generally acting as microRNA (miRNA) sponges to regulate downstream genes expression. However, the aberrant expression profile and dysfunction of circRNAs in human bladder cancer remain to be investigated. The present study aims to elucidate the potential role and molecular mechanism of circACVR2A in regulating the proliferation and metastasis of bladder cancer. Methods circACVR2A (hsa_circ_0001073) was identified by RNA-sequencing and validated by quantitative real-time polymerase chain reaction and agarose gel electrophoresis. The role of circACVR2A in bladder cancer was assessed both in vitro and in vivo. Biotin-coupled probe pull down assay, biotin-coupled microRNA capture, dual-luciferase reporter assay, and fluorescence in situ hybridization were conducted to evaluate the interaction between circACVR2A and microRNAs. Results The expression of circACVR2A was lower in bladder cancer tissues and cell lines. The down-regulation of circACVR2A was positively correlated with aggressive clinicopathological characteristics, and circACVR2A served as an independent risk factor for overall survival in bladder cancer patients after cystectomy. Our in vivo and in vitro data indicated that circACVR2A suppressed the proliferation, migration and invasion of bladder cancer cells. Mechanistically, we found that circACVR2A could directly interact with miR-626 and act as a miRNA sponge to regulate EYA4 expression. Conclusions circACVR2A functions as a tumor suppressor to inhibit bladder cancer cell proliferation and metastasis through miR-626/EYA4 axis, suggesting that circACVR2A is a potential prognostic biomarker and therapeutic target for bladder cancer. Electronic supplementary material The online version of this article (10.1186/s12943-019-1025-z) contains supplementary material, which is available to authorized users.

Matrine may be used to treat prostate cancer patients to increase the levels of GADD45B to inhibit tumor invasion and improve patient survivals.

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Bladder acellular matrix graft-alginate dialdehyde-gelatin hydrogel-silk mesh (BAMG-HS) encapsulated with adipose-derived stem cells (ASCs) was evaluated in a rat model of augmentation cystoplasty, including BAMG-HS-ASCs (n = 18, subgroup n = 6 for 2, 4, and 12 weeks), acellular BAMG-HS (n = 6 for 12 weeks) and cystotomy control (n = 6 for 12 weeks) groups. Equipped with good cytocompatibility and superior mechanical properties (elastic modulus: 5.33 ± 0.96 MPa, maximum load: 28.90 ± 0.69 N), BAMG-HS acted a trilayer "sandwich" scaffold with minimal interference in systemic homeostasis. ASCs in BAMG-HS promoted morphological and histological bladder restoration by accelerating scaffold degradation (p < 0.05), ameliorating fibrosis (p < 0.05) and inflammation (p < 0.01). Additionally, ASCs facilitated the recovery of bladder function by enhancing smooth muscle regeneration (p < 0.05), innervation (p < 0.01) and angiogenesis (p < 0.001). Except for a small number of endothelium-differentiated ASCs, the pro-angiogenic effects of ASCs were mainly related to ERK1/2 phosphorylation in the downstream of SDF-1α/CXCR4 pathway.