Evidence map›Paper›PMID 28921383›Full record

ArticleDigestive diseases and sciences2017

LncRNA-CCAT1 Promotes Migration, Invasion, and EMT in Intrahepatic Cholangiocarcinoma Through Suppressing miR-152.

Shouhua Zhang, Juhua Xiao, Yong Chai, Yun Yan Du, Zhiqiang Liu, Kai Huang, Xin Zhou, Wei Zhou

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.2field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

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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

42 citing papers in PubMed, 64 citations in OpenAlex.

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  10. Long Non-Coding RNAs as Molecular Biomarkers in Cholangiocarcinoma.Frontiers in cell and developmental biology · 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

8 authors at 4 institutions in 1 country.

Shouhua ZhangDepartment of General Surgery, Jiangxi Children's Hospital, Nanchang, 330006, Jiangxi Province, China.
Juhua XiaoDepartment of Ultrasound, Jiangxi Provincial Maternal and Child Health Hospital, Nanchang, 330006, Jiangxi Province, China.
Yong ChaiDepartment of General Surgery, Jiangxi Children's Hospital, Nanchang, 330006, Jiangxi Province, China.
Yun Yan DuDepartment of Otolaryngology, Jiangxi Provincial People's Hospital, Nanchang, 330006, Jiangxi Province, China.
Zhiqiang LiuDepartment of General Surgery, Jiangxi Children's Hospital, Nanchang, 330006, Jiangxi Province, China.
Kai HuangDepartment of Gastrointestinal Surgery, Jiangxi Provincial Cancer Hospital, No. 519, Beijing East Road, Nanchang, 330029, Jiangxi Province, China.
Xin ZhouDepartment of Ultrasound, Jiangxi Provincial Maternal and Child Health Hospital, Nanchang, 330006, Jiangxi Province, China.
Wei ZhouDepartment of Gastrointestinal Surgery, Jiangxi Provincial Cancer Hospital, No. 519, Beijing East Road, Nanchang, 330029, Jiangxi Province, China. weizhou1976@126.com.
Jiangxi Provincial Children's Hospital · CNJiangxi Maternal and Child Health Hospital · CNJiangxi Provincial Cancer Hospital · CNJiangxi Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence has suggested that lncRNA CCAT1 is upregulated and functions as a potential tumor promoter in many cancers. However, the potential biological roles and regulatory mechanisms of CCAT1 in intrahepatic cholangiocarcinoma (ICC) remain unclear.

methodsWe used real-time PCR to measure CCAT1 expression in ICC tissues and the adjacent normal tissues. The statistical analyses were applied to evaluate the prognostic value and associations of CCAT1 expression with clinical parameters. The CCAT1 was silenced with siRNA in ICC cells. The migration and invasion of ICC cells were detected with Transwell assay. The expressions of epithelial-mesenchymal transition (EMT)-related proteins were evaluated to discover whether the process of EMT was involved.

resultsWe found that CCAT1 expression was elevated in ICC tissues compared to the adjacent normal tissues. We also found that high CCAT1 expression is closely correlated with tumor progression in ICC patients. Furthermore, our results show that knockdown of CCAT1 significantly suppressed the migration and invasion of ICC cells. Additionally, CCAT1 silencing remarkably reverses the EMT phenotype of ICC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that CCAT1 directly bound to the miR-152, which has been reported to serve as a tumor suppressor in variety cancers. Further investigation demonstrated that CCAT1 led to the metastasis and EMT activation of ICC cells through inhibiting miR-152.

conclusionsOur results suggested that CCAT1 functions as an oncogenic lncRNA in ICC, which could serve as a potential diagnostic and therapeutic target for ICC patients.

Indexed as

Cell MovementEpithelial-Mesenchymal Transition3' Untranslated RegionsBile Duct NeoplasmsBinding SitesCell Line, TumorCholangiocarcinomaComputational BiologyDatabases, GeneticDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMaleMicroRNAsMiddle Aged3' Untranslated RegionsCCAT1 long noncoding RNA, humanMicroRNAsMIRN152 microRNA, humanRNA, Long NoncodingEMTIntrahepatic cholangiocarcinomaInvasionlncRNA-CCAT1miR-152

Identifiers

PMID28921383
OpenAlexW2756293922

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Registered trials

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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.