Evidence map›Paper›PMID 29506532›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

CADM2, as a new target of miR-10b, promotes tumor metastasis through FAK/AKT pathway in hepatocellular carcinoma.

Dongliang Li, Yongjian Zhang, He Zhang, Chao Zhan, Xin Li, Tu Ba, Zini Qiu, Fang E, Guixiang Lv, Chendan Zou and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

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  16. Genome-wide Interaction Study with Smoking for Colorectal Cancer Risk Identifies Novel Genetic Loci Related to Tumor Suppression, Inflammation, and Immune Response.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023
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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

15 authors at 5 institutions in 1 country.

Dongliang LiDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Yongjian ZhangDepartment of Hepatobiliary and Pancreas, Heilongjiang Cancer Hospital, Harbin, China.
He ZhangDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Chao ZhanDepartment of Hepatobiliary and Pancreas, Heilongjiang Cancer Hospital, Harbin, China.
Xin LiDepartment of Respiratory Medical Oncology, Heilongjiang Cancer Hospital, Harbin, China.
Tu BaDepartment of Neck and Breast Surgery, Mudanjiang Tumor Hospital, Mudanjiang, China.
Zini QiuDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Fang EDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Guixiang LvDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Chendan ZouDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Chuxuan WangDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Lining SiDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.
Chaoxia ZouDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China. zouchaoxia006@126.com.
Qiang LiDepartment of General Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, China. lq_79224@163.com.
Xu GaoDepartment of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, China. gaoxu_671227@163.com.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CNHeilongjiang Academy of Sciences · CNMudanjiang Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CN

Funding

Application research and development plan major project of Heilongjiang GA16C105China Postdoctoral Science Foundation 2015M581479National Natural Science Foundation of China 81572347National Natural Science Foundation of China 81773165Natural Science Foundation of Heilongjiang for the Returned Overseas Chinese Scholars LC2016029
6 · The paper itself

Abstract

backgroundCell adhesion molecules (CADMs) comprise of a protein family whose functions include maintenance of cell polarity and tumor suppression. Hypo-expression of CADM2 gene expression has been observed in several cancers including hepatocellular carcinoma (HCC). However, the role and mechanisms of CADM2 in HCC remain unclear.

methodsThe expression of CADM2 and miRNA-10b (miR-10b) in HCC tissues and cell lines were detected using real-time PCR and Western blotting. Immunofluorescence was used to detect Epithelial-mesenchymal transition (EMT) progression in HCC cell lines. Dual-luciferase reporter assay was used to determine miR-10b binding to CADM2 3'UTR. Wound healing assay and Transwell assay were performed to examine the migration and invasion of HCC cells.

resultsWe report the effect of CADM2 as a tumor suppressor in HCC. Firstly, we confirmed that CADM2 expression was significantly down regulated in HCC tissues compared to normal tissues according to TCGA data analysis and fresh HCC sample detection. Secondly, overexpression of CADM2 could inhibit EMT process, migratory and invasion ability of HCC cells. Furthermore, the results indicated that CADM2 is a direct target of miR-10b in HCC cells and miR-10b/CADM2 modulates EMT process and migration ability via focal adhesion kinase (FAK) /AKT signaling pathway in HCC.

conclusionsOur study demonstrates that miR-10b-CADM2-FAK/AKT axis plays an important role in HCC metastasis, which might be a novel potential therapeutic option for HCC treatment.

Indexed as

Gene Expression Regulation, NeoplasticSignal Transduction3' Untranslated RegionsCarcinoma, HepatocellularCell Adhesion MoleculesCell MovementEpithelial-Mesenchymal TransitionFocal Adhesion Protein-Tyrosine KinasesGene ExpressionGenes, ReporterHumansLiver NeoplasmsMicroRNAsModels, BiologicalNeoplasm MetastasisNeoplasm Staging3' Untranslated RegionsCADM2 protein, humanCell Adhesion MoleculesFocal Adhesion Protein-Tyrosine KinasesMicroRNAsMIRN10 microRNA, humanProto-Oncogene Proteins c-aktCell adhesion molecule 2Epithelial-mesenchymal transitionHepatocellular carcinomaMicroRNA-10bTumor metastasis

Identifiers

PMID29506532
PMCPMC5836378
OpenAlexW2801829353

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.