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MTA1 expression in human cancers – Clinical and pharmacological significance

Remarkably, majority of the cancer deaths are due to metastasis, not because of primary tumors. Metastasis is one of the important hallmarks of cancer. During metastasis invasion of primary tumor cells from the site of origin to a new organ occurs. Metastasis associated proteins (MTAs) are a small f...

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Bibliographic Details
Published in:Biomedicine & pharmacotherapy 2017-11, Vol.95, p.956-964
Main Authors: Malisetty, Vijaya Lakshmi, Penugurti, Vasudevarao, Panta, Prashanth, Chitta, Suresh Kumar, Manavathi, Bramanandam
Format: Article
Language:English
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Summary:Remarkably, majority of the cancer deaths are due to metastasis, not because of primary tumors. Metastasis is one of the important hallmarks of cancer. During metastasis invasion of primary tumor cells from the site of origin to a new organ occurs. Metastasis associated proteins (MTAs) are a small family of transcriptional coregulators that are closely associated with tumor metastasis. These proteins are integral components of nuclear remodeling and deacetylation complex (NuRD). By virtue of being integral components of NuRD, these proteins regulate the gene expression by altering the epigenetic changes such as acetylation and methylation on the target gene chromatin. Among the MTA proteins, MTA1 expression is very closely correlated with the aggressiveness of several cancers that includes breast, liver, colon, pancreas, prostate, blood, esophageal, gastro-intestinal etc. Considering its close association with aggressiveness in human cancers, MTA1 may be considered as a potential therapeutic target for cancer treatment. The recent developments in its crystal structure further strengthened the idea of developing small molecule inhibitors for MTA1. In this review, we discuss the recent trends on the diverse functions of MTA1 and its role in various cancers, with the focus to consider MTA1 as a ‘druggable’ target in the control of human cancers.
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2017.09.025