Evidence map›Paper›PMID 27009809›Full record

ArticleOncotarget2016

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, Xue-Nong Li

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 61 citations in OpenAlex.

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  4. Expression ofMolecular medicine reports · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Zuo-Yang ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Yan-Xia LuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Zhe-Ying ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Ya-Ya ChangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Lin ZhengDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Li YuanDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Fan ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Yu-Han HuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Wen-Juan ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Xue-Nong LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Southern Medical University · CNGuangzhou Women and Children Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsCell ProliferationColorectal NeoplasmsEpithelial Cell Adhesion MoleculeHCT116 CellsHeterograftsHumansMiceMice, NudeNeoplasm InvasivenessRNA, Long NoncodingEPCAM protein, humanEpithelial Cell Adhesion MoleculeRNA, Long NoncodingTINCR lncRNA, humanc-Myccolorectal cancerEpCAMsp1TINCR

Identifiers

PMID27009809
PMCPMC5008388
OpenAlexW2299317371

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.