title: Molecular functions and significance of the MTA family in hormone-independent cancer.
abstract: The members of the metastasis-associated protein (MTA) family play pivotal roles in both physiological and pathophysiological processes, especially in cancer development and metastasis, and their role as master regulators has come to light. Due to the fact that they were first identified as crucial factors in estrogen receptor-mediated breast cancer metastasis, most of the early studies focused on their hormone-dependent functions. However, the accumulating evidence shows that the members of MTA family are deregulated in most, if not all, the cancers studied so far. Therefore, the levels as well as the activities of the MTA family members are widely accepted as potential biomarkers for diagnosis, prognosis, and predictors of overall survival. They function differently in different cancers with specific mechanisms. p53 and HIF-1α appear to be the respectively common upstream and downstream regulator of the MTA family in both development and metastasis of a wide spectrum of cancers. Here, we review the expression and clinical significance of the MTA family, focusing on hormone-independent cancers. To illustrate the molecular mechanisms, we analyze the MTA family-related signaling pathways in different cancers. Finally, targeting the MTA family directly or the pathways involved in the MTA family indirectly could be invaluable strategies in the development of cancer therapeutics.
authors.affiliation: Laboratory for Translational Oncology, Basic Medicine College, Hubei University of Science and Technology, Xianning, Hubei Province, 437100, China.
authors.forename: Zhifeng
authors.initials: Z
authors.lastname: Ning
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Gan
authors.forename: Chaoying
authors.initials: C
authors.lastname: Chen
authors.forename: Dianzheng
authors.initials: D
authors.lastname: Zhang
authors.forename: Hao
authors.initials: H
authors.lastname: Zhang
mesh_terms: D015972:Gene Expression Regulation, Neoplastic; D006655:Histone Deacetylases / Q000096:biosynthesis / Q000235:genetics*; D006728:Hormones / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics; D056245:Mi-2 Nucleosome Remodeling and Deacetylase Complex / Q000235:genetics; D058990:Molecular Targeted Therapy; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology / Q000628:therapy; D011379:Prognosis; D012097:Repressor Proteins / Q000096:biosynthesis / Q000235:genetics*; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53 / Q000235:genetics
chemical_list: C497442:HIF1A protein, human; D006728:Hormones; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; C486657:MTA3 protein, human; C089320:MTA1 protein, human; D009363:Neoplasm Proteins; D012097:Repressor Proteins; C495901:TP53 protein, human; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53; C120917:MTA2 protein, human; D006655:Histone Deacetylases; D056245:Mi-2 Nucleosome Remodeling and Deacetylase Complex