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Analyses of our previously determined microRNA (miRNA) expression signature of renal cell carcinoma (RCC) and The Cancer Genome Atlas (TCGA) database revealed that both strands of the pre-miR-532-duplex-miR-532-5p (the guide strand) and miR-532-3p (the passenger strand)- are closely associated with poor prognosis of RCC patients (P = 0.0411 and P = 0.022, respectively). In this study we investigated the functional significance of these miRNAs and identified gene targets involved in RCC pathogenesis. Ectopic expression of these miRNAs significantly attenuated the malignant phenotypes including proliferation, migration and invasion of two RCC cell lines, 786-O and A498. A combination of genome-wide gene expression and in silico database analyses revealed 36 and 34 genes as putative target oncogenes regulated by miR-532-5p and miR-532-3p, respectively, in RCC cells. Among these targets, expression of aquaporin9 (AQP9), a water channel protein, was directly regulated by both miR-532-5p and miR-532-3p, and high expression levels of AQP9 were significantly associated with poor prognosis of RCC patients (P = 2.03e-05). Multivariate analysis indicated that AQP9 expression is an independent prognostic factor for RCC patients. Aberrant AQP9 expression at both the gene and protein level was detected in RCC clinical specimens. siRNA-mediated knockdown of AQP9 by si-AQP9 inhibited the malignant phenotypes of RCC cells. Rescue assays of AQP9 overexpression showed that the miR-532/AQP9 axis was closely involved in RCC oncogenesis. The identification of antitumor miRNAs and their targets will contribute to an increased understanding of the molecular pathogenesis of RCC.
microRNA, antitumor, miR-532-5p, miR-532-3p, passenger strand, renal cell carcinoma, AQP9
Role of pre-miR-532 (miR-532-5p and miR-532-3p) in regulation of gene expression and molecular pathogenesis in renal cell carcinoma
Yasutaka Yamada,1,2 Takayuki Arai,1,2 Mayuko Kato,1,2 Satoko Kojima,3 Shinichi Sakamoto,2 Akira Komiya,2 Yukio Naya,3 Tomohiko Ichikawa,2 and Naohiko Seki1
Despite the fact that miRNAs play pivotal roles in various human malignancies, their molecular mechanisms influencing RCC are poorly understood.
The expression of miRNAs from RCC and paired normal renal specimens was analysed by a combined computational and experimental approach using two published datasets and qRT-PCR assays. The functional role of these miRNAs was further identified by overexpression and inhibition assays in vivo and in vitro. Western blots, luciferase assays, and chromatin immunoprecipitation were performed to investigate the potential mechanisms of these miRNAs.
Bioinformatics analysis and qRT-PCR revealed that miR-532-5p was one of the most heavily downregulated miRNAs. Overexpression of miR-532-5p inhibited RCC cell proliferation, while knockdown of miR-532-5p promoted cell proliferation. Mechanistic analyses indicated that miR-532-5p directly targets KRAS and NAP1L1. Interestingly, ETS1 suppressed the transcription of miR-532-5p by directly binding a special region of its promoter. Moreover, high levels of ETS1, as an oncogene in RCC, were significantly associated with poor survival in a large cohort of RCC specimens.
Our work presents a road map for the prediction and validation of a miR-532-5p/KRAS-NAP1L1/P-ERK/ETS1 axis feedback loop regulating cell proliferation, which could potentially provide better therapeutic avenues for treating RCC.
Subject terms: Cell growth, Tumour biomarkers, miRNAs
MiR-532-5p suppresses renal cancer cell proliferation by disrupting the ETS1-mediated positive feedback loop with the KRAS-NAP1L1/P-ERK axis
Wei Zhai,corresponding author#1 Junjie Ma,#2 Rujian Zhu,#2,3 Chen Xu,4 Jin Zhang,1 Yonghui Chen,1 Zhiguo Chen,4 Dongkui Gong,4 Jiayi Zheng,5 Chen Chen,2 Saiyang Li,2 Butang Li,1 Yiran Huang,1 Wei Xue,corresponding author1 and Junhua Zhengcorresponding author6
2018 Aug 28;
The expression panel of plasma microRNA defined miR-532-3p as a valuable biomarker for colorectal adenoma (CRA). However, its expression pattern and function in colorectal cancer (CRC) have remained unclear. The present study investigated the expression levels of miR-532-3p and found that it was in situ downregulated both in CRA and CRC. Moreover, it functioned as a sensitizer for chemotherapy in CRC by inducing cell cycle arrest and early apoptosis via its activating effects on p53 and apoptotic signaling pathways. In addition, miR-532-3p was found to restrain cell growth, metastasis, and epithelial-mesenchymal transition (EMT) phenotype of CRC. A study on the mechanism behind these effects revealed that miR-532-3p directly binds to 3′UTR regions of ETS1 and TGM2, ultimately repressing the canonical Wnt/β-catenin signaling. Further investigation showed that TGM2 was transcriptionally regulated by ETS1 and ETS1/TGM2 axis served as a vital functional target of miR-532-3p in suppressing CRC progression. To conclude, miR-532-3p mimics could act as potential candidate for molecular therapy in CRC through inactivation of the canonical Wnt/β-catenin signaling and enhancement of chemosensitivity.
Subject terms: Colorectal cancer, Oncogenes
MiR-532-3p suppresses colorectal cancer progression by disrupting the ETS1/TGM2 axis-mediated Wnt/β-catenin signaling
Chuncai Gu,#1 Jianqun Cai,#1 Zhijun Xu,#2 Shiming Zhou,1 Liangying Ye,1 Qun Yan,1 Yue Zhang,1 Yuxin Fang,1 Yongfeng Liu,1 Chenge Tu,1 Xinke Wang,1 Juan He,1 Qingyuan Li,1 Lu Han,1 Xin Lin,1 Aimin Li,corresponding author1 and Side Liucorresponding author1