J Cancer 2018; 9(3):521-527. doi:10.7150/jca.22355

Review

Overexpression of MICAL2, a novel tumor-promoting factor, accelerates tumor progression through regulating cell proliferation and EMT

Yongqiang Cai, Jinping Lu, Faqing Tang

Clinical Laboratory and Medical Research Center, Zhuhai Hospital, Jinan University, Zhuhai 519000, Guangdong, China

Abstract

Molecule interacting with CasL 2 (MICAL2), a microtubule associated monooxygenase, is involved in cell growth, axon guidance, vesicle trafficking and apoptosis. Recent studies have demonstrated that MICAL2 is highly expressed in tumor and accelerates tumor progression and it is deemed to be a novel tumor-promoting factor. MICAL2 overexpression increases cell proliferation to accelerate tumor growth, and MICAL2 also promotes epithelial-mesenchymal transition (EMT)-related proteins to increase cancer cell metastasis. On mechanism, MICAL2 induces EMT by regulating SRF (serum response factor)/MRTF-A (myocardin related transcription factor A) signaling, Semaphorin/Plexin pathway and inducing ROS (Reactive oxygen species) production. In the present review, we introduced MICAL family, expatiated the structure and functions of MICALs, and summarized the mechanisms of MICAL2 involving tumor progression. The challenges and perspectives for MICAL2 in tumor are also discussed.

Keywords: MICAL2, cancer, epithelial-mesenchymal transition, metastasis.

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How to cite this article:
Cai Y, Lu J, Tang F. Overexpression of MICAL2, a novel tumor-promoting factor, accelerates tumor progression through regulating cell proliferation and EMT. J Cancer 2018; 9(3):521-527. doi:10.7150/jca.22355. Available from http://www.jcancer.org/v09p0521.htm