Evidence map›Paper›PMID 38991944›Full record

ArticleJournal of gynecologic oncology2025

ATF1 regulates MAL2 expression through inhibition of miR-630 to mediate the EMT process that promotes cervical cancer cell development and metastasis.

Yanming Cao, Yuping Peng, Youqun Tang

Abstract read
In one paragraph

Article in Journal of gynecologic oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Yanming CaoDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, China.ORCID 0009-0002-3783-3498
Yuping PengDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, China.ORCID 0009-0007-7572-7457
Youqun TangDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, China. Tangyqun51@163.com.ORCID 0009-0007-5331-4598

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe existence of activating transcription factor 1 (ATF1) could be employed as a clinical marker in the context of cervical cancer development, although its specific mechanism has not been fully clarified.

methodsTo evaluate the presence of ATF1, miR-630, and myelin and lymphocyte protein 2 (MAL2) in cervical malignancies, we conducted quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot assays; further studied the expansion, migration, invasion and epithelial-mesenchymal transition (EMT) of cervical carcinoma cells using colony formation assay, transwell, loss cytometry, Western blot. Chromatin immunoprecipitation (ChIP) and RNA immunoprecipitation (RIP) were used to verify that ATF1 could directly transcriptionally repress miR-630; dual luciferase reporter assay and RIP assay were employed to confirm that miR-630 targeted to repress MAL2.

resultsIn cervical cancer cases, elevated ATF1 expression and reduced miR-630 expression were detected, displaying a negative relationship between them. Inhibition of ATF1 hindered the growth, migration, infiltration, and EMT in cervical carcinoma cells, while upregulation of miR-630 mitigated the aggressive characteristics of these cells. ATF1 was found to transcriptionally repress miR-630 by TransmiR and ALGGEN prediction and ChIP validation. MicroRNA modulates gene expression and affects cancer progression, and we discovered that miR-630 regulates cancer progression by targeting and inhibiting MAL2.

conclusionATF1, which modulates the miR-630/MAL2 pathway, affects the EMT process and cervical carcinoma cell growth and spread. Therefore, ATF1 may serve as a promising marker and treatment target for cervical malignancies intervention.

Indexed as

Activating Transcription Factor 1MicroRNAsMyelin and Lymphocyte-Associated Proteolipid ProteinsUterine Cervical NeoplasmsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasm MetastasisActivating Transcription Factor 1ATF1 protein, humanMicroRNAsMIRN630 microRNA, humanMyelin and Lymphocyte-Associated Proteolipid ProteinsActivating Transcription Factor 1Cervical CancerEpithelial-Mesenchymal TransitionMetastasis

Identifiers

PMID38991944
PMCPMC11790996

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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.