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REVIEW article

Front. Oncol.
Sec. Cancer Molecular Targets and Therapeutics
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1451130

The Role of ESRP1 in Solid Tumor Development through the Regulation of CD44 Splicing and EMT Processes

Provisionally accepted
  • The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China

The final, formatted version of the article will be published soon.

    According to the World Health Organization's statistics, cancer is the second leading cause of death worldwide, following cardiovascular diseases. Despite significant progress in the field of cancer treatment in recent years, cancer remains one of the main factors shortening human life expectancy. The field of cancer research is increasingly focusing on the role of tumor-related oncogenes and heterogeneous proteins in the development of cancer. Studies indicate that there is a close connection between solid tumors and ESRP1. ESRP1 is a key intracellular molecule that plays a crucial role in cell growth and differentiation. As an emerging biomarker, ESRP1 has a decisive impact on the formation and development of solid tumors by regulating the alternative splicing of CD44 and the epithelial-mesenchymal transition (EMT) process. Research shows that abnormal expression of ESRP1 is closely related to the formation and development of various solid tumors, including breast cancer, lung cancer, stomach cancer, and others, and is closely associated with the invasiveness, metastasis, and poor prognosis of tumors. Therefore, given ESRP1's critical role in cancer development, it is gradually becoming a potential biomarker and therapeutic target. This review primarily discusses the molecular mechanisms of ESRP1 in regulating cancer metastasis, particularly its regulatory effects on CD44 splicing and the EMT process. These research findings provide new targets for cancer treatment, aiming to bring more precise diagnosis and more effective treatment strategies to patients.

    Keywords: ESRP1, CD44, EMT, Alternative Splicing, Solid tumor

    Received: 18 Jun 2024; Accepted: 14 Jan 2025.

    Copyright: © 2025 Wang, Zhang, Zhao, Yuan, Zhao, Liu, Ji and Lu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Lili Wang, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China
    Lei Ke Zhao, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China
    Yanting Liu, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China
    Yinghua Ji, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China
    Ping Lu, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.