Oncotarget

Research Papers:

Loss of TINCR expression promotes proliferation, metastasis through activating EpCAM cleavage in colorectal cancer

Zuo-yang Zhang, Yan-xia Lu, Zhe-ying Zhang, Ya-ya Chang, Lin Zheng, Li Yuan, Fan Zhang, Yu-han Hu, Wen-juan Zhang and Xue-nong Li _

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Oncotarget. 2016; 7:22639-22649. https://doi.org/10.18632/oncotarget.8141

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Abstract

Zuo-yang Zhang1,*, Yan-xia Lu1,*, Zhe-ying Zhang1, Ya-ya Chang1, Lin Zheng1, Li Yuan1,2, Fan Zhang1, Yu-han Hu1, Wen-juan Zhang1, Xue-nong Li1

1Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China

2Department of Pathology, Guangzhou Women and Children’s Medical Center, Guangzhou 510515, China

*These authors contributed equally to this work

Correspondence to:

Xue-nong Li, e-mail: [email protected]

Keywords: TINCR, EpCAM, c-Myc, sp1, colorectal cancer

Received: November 03, 2015     Accepted: February 15, 2016     Published: March 17, 2016

ABSTRACT

Long non-coding RNAs (lncRNAs) are involved in kinds of human diseases, including colorectal cancer (CRC). TINCR, a 3.7 kb long non coding RNA, was associated with cell differentiation in keratinocyte and gastric cancer cells. However, little is known about the role of TINCR in regulation CRC progression. Here, we showed that lncRNA TINCR was associated with CRC proliferation and metastasis. TINCR was statistically downregulated in CRC tissues and metastatic CRC cell lines compared with their counterparts. TINCR was reversely correlated with CRC progression and promoted tumor cells growth, metastasis in vivo and in vitro. While overexpression of TINCR had opposite effect. In addition, we also found that TINCR specifically bound to EpCAM through RNA IP and RNA pull down assays. Loss of TINCR promoted hydrolysis of EpCAM and then released EpICD, subsequently, activated the Wnt/β-catenin pathway. Further studies shown that c-Myc repressed the expression of TINCR through repressing sp1 transcriptive activity, which established a positive feedback loop controlling c-Myc and TINCR expression. These findings elucidate that loss of TINCR expression promotes proliferation and metastasis in CRC and it could be considered as a potential cancer suppressor gene.


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