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

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

Author information

1
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.
2
Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
3
Department of Urology and Transplantation, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
4
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.
5
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. Electronic address: dr_tangjy@163.com.
6
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. Electronic address: malong1997@sina.com.

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.

KEYWORDS:

Bladder cancer; Invasion; LINC00536; Migration; Proliferation; Wnt3a

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