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Biosci Rep. 2018 Sep 5;38(5). pii: BSR20180562. doi: 10.1042/BSR20180562. Print 2018 Oct 31.

High LINC01605 expression predicts poor prognosis and promotes tumor progression via up-regulation of MMP9 in bladder cancer.

Author information

1
Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, China.
2
Department of Urology, Jiangsu Province Hospital of TCM, Affiliated Hospital of Nanjing University of TCM, Nanjing 210029, China.
3
Department of Urology, Affiliated Hospital of Nantong University, Nantong 226001, China xingqianwei@ntu.edu.cn yj197912@163.com.
4
Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, China xingqianwei@ntu.edu.cn yj197912@163.com.

Abstract

The advent of high-throughput sequencing methods has facilitated identification of novel long non-coding RNAs (lncRNAs), which have been demonstrated to play an important role in multiple tumors. Moreover, with the assistance of bioinformatics analysis, LINC01605 has been found to be up-regulated in bladder cancer (BC) tissues compared with normal tissues. Hence, the present study was to explore its specific biological role and related mechanism in BC. The relative expression level of LINC01605 was measured in a cohort of BC tissues with matched normal tissues as well as human BC cell lines by quantitative real-time PCR (qRT-PCR). Survival analysis was performed to explore the relationship between LINC01605 expression and the prognosis of BC patients. The biological function of LINC01605 was studied in vitroand in vivo, by means of CCK-8 assay, colony formation assay, transwell assay, and tumor xenografts mice model. LINC01605 was found to be frequently highly expressed in both human BC cells and tissues. Survival analysis indicated that high LINC01605 expression was associated with higher histological grade and clinical stages. In addition, down-regulated LINC01605 in BC cells could significantly inhibit the abilities of proliferation, migration, and invasion in vitro and knockdown of LINC01605 in subcutaneous xenograft tumor model could impede tumorigenesis in vivo Mechanistically, LINC01605 could activate epithelial-mesenchymal transition (EMT) signaling pathway and promote the expression of matrix metallopeptidase (MMP) 9 (MMP9). In summary, our results shed light on that LINC01605, as a new prognostic biomarker, could promote the proliferation, migration, and invasion of BC cells via activating EMT signaling pathway and up-regulating MMP9 expression.

KEYWORDS:

Bladder cancer; EMT; MMP9; Migration; lncRNA LINC01605

PMID:
30054424
PMCID:
PMC6123067
DOI:
10.1042/BSR20180562
[Indexed for MEDLINE]
Free PMC Article

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