%0 Generic %A Zhang, Wentao %A Mao, Shiyu %A Shi, Donghui %A Zhang, Junfeng %A Zhang, Ziwei %A Guo, Yadong %A Wu, Yuan %A Wang, Ruiliang %A Wang, Longsheng %A Huang, Yong %A Yao, Xudong %D 2019 %T Table_1_MicroRNA-153 Decreases Tryptophan Catabolism and Inhibits Angiogenesis in Bladder Cancer by Targeting Indoleamine 2,3-Dioxygenase 1.DOCX %U https://frontiersin.figshare.com/articles/dataset/Table_1_MicroRNA-153_Decreases_Tryptophan_Catabolism_and_Inhibits_Angiogenesis_in_Bladder_Cancer_by_Targeting_Indoleamine_2_3-Dioxygenase_1_DOCX/8851196 %R 10.3389/fonc.2019.00619.s001 %2 https://frontiersin.figshare.com/ndownloader/files/16214654 %K bladder cancer %K miR-153 %K tryptophan catabolism %K angiogenesis %K indoleamine 2 %K 3-dioxygenase 1 %X

Background: Metastasis is the primary cause of cancer deaths, warranting further investigation. This study assessed microRNA-153 (miR-153) expression in bladder cancer tissues and investigated the underlying molecular mechanism of miR-153-mediated regulation of bladder cancer cells.

Methods: Paired tissue specimens from 45 bladder cancer patients were collected for qRT-PCR. The Cancer Genome Atlas (TCGA) dataset was used to identify associations of miR-153 with bladder cancer prognosis. Bladder cancer tissues and immortalized cell lines were used for the following experiments: miR-153 mimics and indoleamine 2,3-dioxygenase 1 (IDO1) siRNA transfection; Western blot, cell viability, colony formation, and Transwell analyses; nude mouse xenograft; and chicken embryo chorioallantoic membrane angiogenesis (CAM) assays. Human umbilical vein endothelial cells (HUVECs) were co-cultured with bladder cancer cells for the tube formation assay. The luciferase reporter assay was used to confirm miR-153-targeting genes.

Results: miR-153 expression was downregulated in bladder cancer tissues and cell lines, and reduced miR-153 expression was associated with advanced tumor stage and poor overall survival of patients. Moreover, miR-153 expression inhibited bladder cancer cell growth by promoting tumor cell apoptosis, migration, invasion, and endothelial mesenchymal transition (EMT) in vitro and tumor xenograft growth in vivo, while miR-153 expression suppressed HUVEC and CAM angiogenesis. At the gene level, miR-153 targeted IDO1 expression and inhibited bladder cancer cell tryptophan metabolism through inhibiting IL6/STAT3/VEGF signaling.

Conclusions: Collectively, our data demonstrate that miR-153 exerts anti-tumor activity in bladder cancer by targeting IDO1 expression. Future studies will investigate miR-153 as a novel therapeutic target for bladder cancer patients.

%I Frontiers