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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 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is the main pathway investigated in this study?","Question",{"text":63,"@type":64},"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.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How did the researchers assess ATF1, miR-630, and MAL2?",{"text":68,"@type":64},"ATF1, miR-630, and MAL2 levels were measured using quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot assays.",{"name":70,"@type":61,"acceptedAnswer":71},"What functional effects were observed when ATF1 or miR-630 was inhibited or upregulated?",{"text":72,"@type":64},"Inhibition of ATF1 hindered cervical carcinoma cell growth, migration, invasion, and EMT, while upregulation of miR-630 mitigated aggressive cancer cell characteristics.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},329856,1790422247,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,109,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & 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[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  \nOriginal Article  \nReceived: Nov 2, 2023  \nRevised: Apr 3, 2024  \nAccepted: Jun 11, 2024  \nPublished online: Jul 2, 2024  \nCorrespondence to  \nYouqun Tang  \nDepartment of Oncology, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Yuelu District, Changsha 410013, China.  \n[Email: Tangyqun51@163.com](Email: Tangyqun51@163.com)  \n© 2025. Asian Society of Gynecologic Oncology, Korean Society of Gynecologic Oncology, and Japan Society of Gynecologic Oncology  \nThis 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.  \nORCID iDs  \nYanming 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)  \nConflict of Interest  \nNo potential conflict of interest relevant to this article was reported.  \nATF1 regulates MAL2 expression through inhibition of miR-630 to mediate the EMT process that promotes cervical cancer cell development and metastasis  \nYanming Cao , Yuping Peng , Youqun Tang   \nDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, China  \nABSTRACT  \nObjective: 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.  \nMethods: 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 .  \nConclusion: 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.  \nKeywords: Cervical Cancer; Activating Transcription Factor 1; Epithelial-Mesenchymal Transition; Metastasis  \nSynopsis  \nOur study identified the overexpression of ATF1 in cervical cancer patients and revealed its oncogenic effects via the miR-630/MAL2 pathway.  \n[https://ejgo.org](https://ejgo.org) 1/15  \nATF1’s role in cervical cancer spread  \nData Accessibility Statement  \nAll data ","cbCaicEE5Xkjoodo","https://ap.wps.com/l/cbCaicEE5Xkjoodo","pdf",10183515,15,"English","# Abstract\n## Objective\n## Methods\n## Results\n## Conclusion\n# Introduction\n## Global burden and risk factors\n## ATF1 background and rationale","[{\"question\":\"What is the main pathway investigated in this study?\",\"answer\":\"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.\"},{\"question\":\"How did the researchers assess ATF1, miR-630, and MAL2?\",\"answer\":\"ATF1, miR-630, and MAL2 levels were measured using quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot assays.\"},{\"question\":\"What functional effects were observed when ATF1 or miR-630 was inhibited or upregulated?\",\"answer\":\"Inhibition of ATF1 hindered cervical carcinoma cell growth, migration, invasion, and EMT, while upregulation of miR-630 mitigated aggressive cancer cell characteristics.\"}]","ATF1 regulates MAL2 expression through inhibition of miR-630 to mediate the EMT process that promotes cervical cancer cell development and metastasis | PDF",1789985871,38]