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

Sep 21, 2026

Upload by Aurelia

Objective: Activating transcription factor 1 (ATF1) is evaluated as a potential clinical marker for cervical cancer development, while its underlying mechanism remains insufficiently defined. Methods: ATF1, miR-630, and myelin and lymphocyte protein 2 (MAL2) are assessed in cervical malignancies using quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot, alongside functional assays for proliferation, migration, invasion, and EMT. Chromatin immunoprecipitation and RNA immunoprecipitation confirm direct transcriptional repression and miRNA targeting. Results: Cervical cancer shows elevated ATF1 and reduced miR-630 with an inverse relationship; ATF1 inhibition suppresses growth and EMT, whereas miR-630 upregulation reduces aggressive phenotypes. Conclusion: ATF1 modulates the miR-630/MAL2 axis, influencing EMT and metastatic spread, supporting ATF1 as a marker and therapeutic target.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages15

Reading Time38 min

AccessFree to download

Abstract

Objective

Methods

Results

Conclusion

Introduction

Global burden and risk factors

ATF1 background and rationale

J Gynecol Oncol. 2025 Jan;36(1):e11 [https://doi.org/10.3802/jgo.2025.36.e11](https://doi.org/10.3802/jgo.2025.36.e11)[ ](https://doi.org/10.3802/jgo.2025.36.e11)pISSN 2005-0380·eISSN 2005-0399 Original Article Received: Nov 2, 2023 Revised: Apr 3, 2024 Accepted: Jun 11, 2024 Published online: Jul 2, 2024 Correspondence to Youqun Tang Department of Oncology, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Yuelu District, Changsha 410013, China. [Email: Tangyqun51@163.com](Email: Tangyqun51@163.com) © 2025. Asian Society of Gynecologic Oncology, Korean Society of Gynecologic Oncology, and Japan Society of Gynecologic Oncology This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ([https://](https://)[ ](https://)[creativecommons.org/licenses/by-nc/4.0/](creativecommons.org/licenses/by-nc/4.0/)) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ORCID iDs Yanming Cao [https://orcid.org/0009-0002-3783-3498](https://orcid.org/0009-0002-3783-3498)[ ](https://orcid.org/0009-0002-3783-3498)Yuping Peng [https://orcid.org/0009-0007-7572-7457](https://orcid.org/0009-0007-7572-7457)[ ](https://orcid.org/0009-0007-7572-7457)Youqun Tang [https://orcid.org/0009-0007-5331-4598](https://orcid.org/0009-0007-5331-4598) Conflict of Interest No potential conflict of interest relevant to this article was reported. 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 Department of Oncology, The Third Xiangya Hospital of Central South University, Changsha, China ABSTRACT Objective: The 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. Methods: To 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 . Results: In 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 . Conclusion: ATF1, 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. Keywords: Cervical Cancer; Activating Transcription Factor 1; Epithelial-Mesenchymal Transition; Metastasis Synopsis Our study identified the overexpression of ATF1 in cervical cancer patients and revealed its oncogenic effects via the miR-630/MAL2 pathway. [https://ejgo.org](https://ejgo.org) 1/15 ATF1’s role in cervical cancer spread Data Accessibility Statement All data

FAQs

What is the main pathway investigated in this study?

The study focuses on the ATF1–miR-630–MAL2 axis and how it mediates epithelial-mesenchymal transition (EMT) to promote cervical cancer progression and metastasis.

How did the researchers assess ATF1, miR-630, and MAL2?

ATF1, miR-630, and MAL2 levels were measured using quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot assays.

What functional effects were observed when ATF1 or miR-630 was inhibited or upregulated?

Inhibition of ATF1 hindered cervical carcinoma cell growth, migration, invasion, and EMT, while upregulation of miR-630 mitigated aggressive cancer cell characteristics.

Sep 21, 2026

Upload by Aurelia