Evidence map›Paper›PMID 34240323›Full record

ArticleDigestive diseases and sciences2022

microRNA-206 Suppresses Cholangiocarcinoma Cell Growth and Invasion by Targeting Jumonji AT-Rich Interactive Domain 2.

Chunying Xie, Zhenxing Huang, Zhaohui Huang, Xue Zhang, Siyuan Lou

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Article in Digestive diseases and sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 3 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Chunying XieDepartment of Oncology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330000, China.
Zhenxing HuangDepartment of Oncology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330000, China.
Zhaohui HuangDepartment of Oncology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330000, China.
Xue ZhangDepartment of Oncology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330000, China.
Siyuan LouDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Nanchang University, No.1, Minde Road, Nanchang, 330000, China. luochijie79854fbii@163.com.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe current study set out to elucidate the specific role of microRNA (miR)-206 in cholangiocarcinoma (CCA) cell biological activities by negatively modulating jumonji AT-rich interactive domain 2 (JARID2).

methodsFirstly, human intrahepatic biliary epithelial cells and CCA cell lines were selected via the analysis of miR-206 and JARID2 expression patterns in CCA by qRT-PCR. Next, the target relation between miR-206 and JARID2 was predicted by Targetscan and validated using dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay. Subsequently, CCK-8 method, colony formation assay, scratch test, Transwell assay, and western blot analysis were performed to evaluate cancer cell development after the overexpression of miR-206 and/or JARID2, with levels of invasion-related proteins assessed. In addition, xenograft transplantation was also employed to confirm the role of miR-206 in vivo. Lastly, Ki-67 expression pattern was also quantified with immunohistochemistry.

resultsIt was found that miR-206 was poorly expressed and JARID2 was highly expressed in CCA cell lines. Also, miR-206 overexpression brought about a suppressive effect on cancer cell proliferation, migration, and invasion. Furthermore, miR-206 was observed to target JARID2. Meanwhile, JARID2 overexpression promoted cell growth, while simultaneous overexpression of miR-206 and JARID2 impeded malignant cancer progression, indicating that miR-206 overexpression inhibited cell progression via targeting JARID2. Finally, in vivo experimentation illustrated that miR-206 overexpression suppressed tumor growth and weight, and inhibited the expressions of JARID2 N-cadherin, vimentin, and Ki-67.

conclusionAltogether, our findings clarified that miR-206 inhibited CCA malignancy by negatively regulating JARID2.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaMicroRNAsBile Ducts, IntrahepaticCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansKi-67 AntigenPolycomb Repressive Complex 2JARID2 protein, humanKi-67 AntigenMicroRNAsMIRN206 microRNA, humanPolycomb Repressive Complex 2CholangiocarcinomaInvasionJARID2microRNA-206MigrationProliferation

Identifiers

PMID34240323
OpenAlexW3180248748

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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.