The expression of metastasis associated protein 2 in normal development and cancers: mechanism and clinical significance

TL;DR

This paper reviews the role of metastasis-associated protein 2 (MTA2) in normal development and cancer, highlighting its complex functions and potential as a cancer treatment target.

Contribution

The paper provides a comprehensive review of MTA2's mechanisms and clinical significance in development and cancer, emphasizing its dual and sometimes conflicting roles.

Findings

MTA2 is amplified in several cancers and is associated with tumor migration, invasion, and poor prognosis.

MTA2 modulates downstream targets like cell growth and angiogenesis genes, contributing to oncogenic roles.

Conflicting evidence exists regarding MTA2's effect on proliferation in different cancers.

Abstract

Metastasis-associated protein 2 (MTA2), a master transcriptional regulator, through multiple target genes and interacting proteins, has been demonstrated to play a vital role in the regulation of proliferation, replication, apoptosis, autophagy, DNA damage repair, preimplantation, embryonic development and immune cell differentiation. Despite extensive research, the physiological role and pathogenic mechanisms of MTA2 remain poorly understood. Here, we mainly review in the current research the status of MTA2 and its implications in normal development and various tumor biology. Accumulating evidence suggests that MTA2 is frequently amplify in several types of cancers, closely associates with tumor cells migration and invasion, relates to the malignant characteristics and poor prognosis, which therefore has been considered as playing tumor oncogenic roles. Substantial evidence indicates that MTA2 functions by modulating downstream targets including cell growth, invasion as well as angiogenesis related genes. Confusingly, the proliferation effect of MTA2 remains elusive and even conflicting in the development of several solid tumors. Furthermore, we discuss the upstream regulation of MTA2 by transcription factors, microRNAs and lncRNAs in specific physiology and pathology conditions, which results in the abnormal MTA2 expression in various aspects of cancer. In this context, we summarize linked function of MTA2 directly to oncogenesis and might provide a significant avenue for the treatment of diseases. We hope that this review will help tumor molecular biologists further understand the molecular mechanism of MTA2 in normal development and cancer.

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