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高表达 LINC00536 促进膀胱癌的肿瘤进展和预后不良。

High LINC00536 expression promotes tumor progression and poor prognosis in bladder cancer.

机构信息

Department of Urology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, No. 155 Han Zhong Road, Nanjing 210029, China; Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

出版信息

Exp Cell Res. 2019 May 1;378(1):32-40. doi: 10.1016/j.yexcr.2019.03.009. Epub 2019 Mar 6.

DOI:10.1016/j.yexcr.2019.03.009
PMID:30851243
Abstract

Growing evidences demonstrate that long non-coding RNAs (lncRNAs) contribute to the cancer initiation and progression and are considered as promising diagnostic and therapeutic targets of multiple cancers. However, the definite role of LINC00536 in bladder cancer (BC) remains unclear. In the present study, we found LINC00536 expression was highly expressed in BC tissues compared with controls and negatively associated with survival rate in BC patients. Gain-of-function assays indicated that LINC00536 overexpression promoted the proliferation, migration and invasion, whereas LINC00536 knockdown attenuated the cell phenotypes above in BC cell lines. In vivo assay illustrated that LINC00536 knockdown inhibited BC growth in vivo. Mechanistically, Wnt3a was identified as the target of LINC00536. LINC00536 promoted malignant phenotypes via activating the Wnt3a/β-Catenin signaling. Wnt3a knockdown reversed the increase of proliferation, migration, and invasion abilities of BC cells induced by LINC00536 overexpression. In summary, our findings demonstrated that LINC00536 promoted BC progression by modulating the Wnt3a/β-Catenin signaling.

摘要

越来越多的证据表明,长非编码 RNA(lncRNA)有助于癌症的发生和发展,并且被认为是多种癌症有前途的诊断和治疗靶点。然而,LINC00536 在膀胱癌(BC)中的明确作用仍不清楚。在本研究中,我们发现与对照相比,LINC00536 在 BC 组织中表达水平升高,并且与 BC 患者的生存率呈负相关。功能获得实验表明,LINC00536 的过表达促进了 BC 细胞系的增殖、迁移和侵袭,而 LINC00536 的敲低则减弱了上述细胞表型。体内实验表明,LINC00536 的敲低抑制了体内 BC 的生长。机制上,Wnt3a 被鉴定为 LINC00536 的靶标。LINC00536 通过激活 Wnt3a/β-连环蛋白信号通路促进恶性表型。Wnt3a 的敲低逆转了 LINC00536 过表达诱导的 BC 细胞增殖、迁移和侵袭能力的增加。总之,我们的研究结果表明,LINC00536 通过调节 Wnt3a/β-连环蛋白信号通路促进了 BC 的进展。

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