Title: SATB1 and 2 in colorectal cancer.
Authors: Brocato, Jason; Costa, Max
Published In Carcinogenesis, (2015 Feb)
Abstract: The special AT-rich sequence-binding proteins 1 and 2 (SATB1/2) are nuclear matrix associated proteins that are transcription factors involved in chromatin remodeling and gene regulation. Expression of the SATB2 gene is tissue-specific, and the only epithelial cells expressing SATB2 are the glandular cells of the lower gastrointestinal tract where its expression is regulated by microRNA-31 (miR-31) and miR-182. SATB2, along with its homolog SATB1, are thought to be involved in various cancers with their roles in this disease being specific to the type of cancer. Colorectal cancer (CRC) provides the largest association of SATB2 with cancer and the roles of SATB2 are better defined and more studied in CRC than in any other cancer type. SATB1 displays a negative association with SATB2 in CRC. The various studies that have investigated the involvement of SATB1 and 2 in CRC have produced consistent findings. Here, we form four major conclusions regarding the role of these proteins in CRC and their potential clinical value: (i) SATB2 is a sensitive marker to distinguish CRC from other cancer types, (ii) Reduced expression of SATB2 in CRC is associated with poor prognosis, (iii) High levels of SATB1 expression facilitate CRC and are associated with poor prognosis and (iv) Overexpression of miR-31 and -182 in CRC leads to more aggressive cancer. This review will describe several of the key investigations that established these conclusions and highlight results that offer opportunities for future research in the treatment and diagnosis of CRC.
PubMed ID: 25543122
MeSH Terms: Chromatin Assembly and Disassembly; Colon/metabolism; Colorectal Neoplasms/genetics; Colorectal Neoplasms/pathology*; Gene Expression Regulation, Neoplastic; Humans; Matrix Attachment Region Binding Proteins/biosynthesis*; Matrix Attachment Region Binding Proteins/genetics; MicroRNAs/biosynthesis*; MicroRNAs/genetics; Prognosis; Transcription Factors/biosynthesis*; Transcription Factors/genetics