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<p>Cancer is the greatest threat to public health worldwide and a major cause of human death. Compared with conventional chemotherapy, agents targeting key oncogenic drivers and signaling mechanisms are becoming an attractive treatment strategy. Molecule interacting with CasL 2 (MICAL2) is a flavin protein monooxygenase family protein that interacts with CasL2 and is involved in cytoskeletal redox regulation, axon-directed regulation, cell transport, and apoptosis. MICAL2 induces F-actin depolymerization through REDOX modification, thereby promoting the expression of epithelial-mesenchymal transition (EMT)-related proteins and inducing cancer cell invasion and proliferation. Mechanistically, MICAL2 induces EMT by regulating the serum response factor (SRF)/myocardin-related transcription factor A (MRTF-A) signaling pathway, and the semaphorin/plexin pathway and inducing reactive oxygen species (ROS) production. Recent studies have shown that MICAL2 is highly expressed in tumors, accelerates tumor progression, and is a novel tumor-promoting factor. This article summarizes recent research findings to review the biological functions of MICAL2, the potential mechanisms related to cancer progression, and discusses the challenges and prospects in this area, providing a new theoretical basis for clinical molecular targeted therapy for cancer.</p>

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The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential

  • 期刊论文

  • 发表日期：

    2025年4月16日

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  • Ruiying Wang,
  • Zhijuan Hou,
  • Xiao Gao,
  • Binyan Wu,
  • Huizheng Hu,
  • Hongpei Wu

摘要

Cancer is the greatest threat to public health worldwide and a major cause of human death. Compared with conventional chemotherapy, agents targeting key oncogenic drivers and signaling mechanisms are becoming an attractive treatment strategy. Molecule interacting with CasL 2 (MICAL2) is a flavin protein monooxygenase family protein that interacts with CasL2 and is involved in cytoskeletal redox regulation, axon-directed regulation, cell transport, and apoptosis. MICAL2 induces F-actin depolymerization through REDOX modification, thereby promoting the expression of epithelial-mesenchymal transition (EMT)-related proteins and inducing cancer cell invasion and proliferation. Mechanistically, MICAL2 induces EMT by regulating the serum response factor (SRF)/myocardin-related transcription factor A (MRTF-A) signaling pathway, and the semaphorin/plexin pathway and inducing reactive oxygen species (ROS) production. Recent studies have shown that MICAL2 is highly expressed in tumors, accelerates tumor progression, and is a novel tumor-promoting factor. This article summarizes recent research findings to review the biological functions of MICAL2, the potential mechanisms related to cancer progression, and discusses the challenges and prospects in this area, providing a new theoretical basis for clinical molecular targeted therapy for cancer.