Wang Ruiying, Hou Zhijuan, Gao Xiao, Wu Binyan, Hu Huizheng, Wu Hongpei
Nuclear Industry 215 Hospital of Shaanxi Province, Shaanxi, China.
Affiliated Hospital of Shaanxi University of Chinese Medicine, Shaanxi, China.
Hum Cell. 2025 Apr 16;38(3):89. doi: 10.1007/s13577-025-01212-z.
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.
癌症是全球公共卫生面临的最大威胁，也是人类死亡的主要原因。与传统化疗相比，靶向关键致癌驱动因素和信号传导机制的药物正成为一种有吸引力的治疗策略。与CasL 2相互作用的分子（MICAL2）是一种黄素蛋白单加氧酶家族蛋白，它与CasL2相互作用，参与细胞骨架氧化还原调节、轴突定向调节、细胞运输和细胞凋亡。MICAL2通过氧化还原修饰诱导F-肌动蛋白解聚，从而促进上皮-间质转化（EMT）相关蛋白的表达，诱导癌细胞侵袭和增殖。从机制上讲，MICAL2通过调节血清反应因子（SRF）/心肌素相关转录因子A（MRTF-A）信号通路、信号素/丛状蛋白通路并诱导活性氧（ROS）产生来诱导EMT。最近的研究表明，MICAL2在肿瘤中高表达，加速肿瘤进展，是一种新的肿瘤促进因子。本文总结了最近的研究结果，以综述MICAL2的生物学功能、与癌症进展相关的潜在机制，并讨论该领域的挑战和前景，为癌症临床分子靶向治疗提供新的理论依据。
