Evidence map›Paper›PMID 29084594›Full record

ArticleJournal of hematology & oncology2017

Role of AP-2α and MAPK7 in the regulation of autocrine TGF-β/miR-200b signals to maintain epithelial-mesenchymal transition in cholangiocarcinoma.

Dawei Zhang, Haiyan Li, Xiaofeng Jiang, Liangqi Cao, Zilong Wen, Xuewei Yang, Ping Xue

Abstract read
In one paragraph

Article in Journal of hematology & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

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  19. Impact of ERK5 on the Hallmarks of Cancer.International journal of molecular sciences · 2019
    Review
  20. TFAP2A Induced KRT16 as an Oncogene in Lung Adenocarcinoma via EMT.International journal of biological sciences · 2019
    Article
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

7 authors.

Dawei ZhangDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangzhou Medical University, No 250 East Changgang Road, Guangzhou, 510260, China.
Haiyan LiDepartment of Breast and Thyroid Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Xiaofeng JiangDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangzhou Medical University, No 250 East Changgang Road, Guangzhou, 510260, China.
Liangqi CaoDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangzhou Medical University, No 250 East Changgang Road, Guangzhou, 510260, China.
Zilong WenDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangzhou Medical University, No 250 East Changgang Road, Guangzhou, 510260, China.
Xuewei YangDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangzhou Medical University, No 250 East Changgang Road, Guangzhou, 510260, China.
Ping XueDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangzhou Medical University, No 250 East Changgang Road, Guangzhou, 510260, China. gyeyxueping@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCholangiocarcinoma (CCA) is characterized by early lymphatic, metastasis, and low survival rate. Epithelial-mesenchymal transition (EMT) is able to induce tumor metastasis. Although the TGF-β/miR-200 signals promote EMT in various types of cancer, the regulatory mechanism in CCA is still unclear.

methodsExpression of miR-200b, TGF-β, and EMT markers were measured in tumor samples and cell lines by qRT-PCR and western blot. CCK8 assay was performed to measure the cell viability. Transwell assay was used to evaluate migration and invasion. The target genes of miR-200b and transcription factor of TGF-β were analyzed using dual-luciferase reporter system.

resultsWe have demonstrated that CCA exhibited remarkable EMT phenotype and miR-200b was reduced in CCA patients (n = 20) and negatively correlated to TGF-β. Moreover, two CCA cells, HCCC, and RBE, with epithelial appearances treated with TGF-β, showed fibroblastic-like cell morphology with downregulated miR-200b expression. Forced expression of miR-200b abrogated TGF-β-induced EMT initiation, with decreased cell proliferation, migration, and invasion in vitro. Also, TFAP2A (encode AP-2α) and MAPK7 were found to be targeted by miR-200b to downregulate EMT and AP-2α inhibited miR-200b by directly promoting transcription of TGFB1. Overexpression of MAPK7 significantly reversed miR-200b-induced inhibition of EMT, migration, and proliferation by increasing the expression of TGF-β, cyclin D1, and Cdk2. Further, the administration of miR-200b induced a remarkably tumor regression in vivo and reduced the effect of TGF-β-related EMT in AP-2α and MAPK7-dependent manner.

conclusionsOur study highlights that miR-200b-based gene therapy is effective in the treatment of CCA.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaEpithelial-Mesenchymal TransitionHumansMitogen-Activated Protein Kinase 7Transcription Factor AP-2TransfectionTransforming Growth Factor betaMAPK7 protein, humanMitogen-Activated Protein Kinase 7Transcription Factor AP-2Transforming Growth Factor betaAP-2αCholangiocarcinomaEMTMAPK7miR-200bTGF-β

Identifiers

PMID29084594
PMCPMC5663068

What Socratic holds

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LicenceCC BY
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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 Socratic graph.