REVIEW article

Front. Cell Dev. Biol.

Sec. Signaling

Volume 13 - 2025 | doi: 10.3389/fcell.2025.1602649

This article is part of the Research TopicUnraveling the Role of Receptor Signaling in Tumorigenesis and Cancer TherapyView all 6 articles

Research progress of ECT2 and RhoA-related signaling pathways in gynecological tumors

Provisionally accepted
Liying  ShengLiying Sheng1Meili  LiangMeili Liang2Yueli  WangYueli Wang2Zhimei  ZhouZhimei Zhou2Yajing  XieYajing Xie2Yumin  KeYumin Ke2*Zhuna  WuZhuna Wu2*
  • 1The Second Affiliated Hospital of Fujian Medical University, Fujian Medical University, Fuzhou, China
  • 2The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China

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

Epithelial Cell Transformation Factor 2 (ECT2) is highly expressed in a variety of cancers, including gynecological tumors. The mislocalization of ECT2 can abnormally activate Ras homolog family member A (RhoA) in the Ras homolog gene family (Rho) Guanine nucleotide Exchange Factor (GEF) family. Activated RhoA binds to Rho-associated protein kinase (ROCK), phosphorylates various target proteins, triggers a cascade reaction, regulates the functions of downstream proteins, and thereby plays an important role in the occurrence and development of tumors. This article reviews the roles of ECT2 and RhoA/ROCK signaling pathways in ovarian cancer, cervical cancer, and endometrial cancer, and summarizes and discusses the research progress of downstream molecules, transduction pathways, and mechanisms related to them. Through comprehensive analysis and summary of the current research results, it is revealed that the ECT2/RhoA/ROCK signaling pathway and related crosstalk pathways play an important role in the occurrence, development, and metastasis of gynecological tumors. This article aims to provide a basis for related research and offer relevant references for the treatment of gynecological tumors in the future.

Keywords: Ect2, RhoA, ROCK, ovarian cancer, cervical cancer, endometrial cancer

Received: 30 Mar 2025; Accepted: 18 Jun 2025.

Copyright: © 2025 Sheng, Liang, Wang, Zhou, Xie, Ke and Wu. 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:
Yumin Ke, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, Fujian Province, China
Zhuna Wu, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, Fujian Province, China

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