Open AccessOncogenic roles of SMARCB 1/ INI 1 and its deficient tumors
Author(s) -
Kohashi Kenichi,
Oda Yoshinao
Publication year - 2017
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13173
Subject(s) - cancer research , biology , immunohistochemistry , wnt signaling pathway , carcinogenesis , hedgehog signaling pathway , signal transduction , tumor progression , chromatin remodeling , chromatin , microbiology and biotechnology , immunology , cancer , gene , genetics
SMARCB 1/ INI 1 is one of the core subunit proteins of the ATP ‐dependent SWI / SNF chromatin remodeling complex, and is identified as a potent and bona fide tumor suppressor. Interactions have been demonstrated between SMARCB 1/ INI 1 and key proteins in various pathways related to tumor proliferation and progression: the p16‐ RB pathway, WNT signaling pathway, sonic hedgehog signaling pathway and Polycomb pathway. Initially, no detectable SMARCB 1/ INI 1 protein expression was found in malignant rhabdoid tumor cells, whereas all other kinds of tumor cells and non‐tumorous tissue showed SMARCB 1/ INI 1 protein expression. Therefore, immunohistochemical testing for the SMARCB 1/ INI 1 antibody has been considered useful in confirming the histologic diagnosis of malignant rhabdoid tumors. However, recently, aberrant expression of SMARCB 1/ INI 1 has been found in various tumors such as epithelioid sarcomas, schwannomatosis, synovial sarcomas, and so on. In addition, it has been reported that aberrant expression can be classified into three patterns: complete loss, mosaic expression and reduced expression. Although the various pathways related to mechanisms of tumorigenesis and tumor proliferation are complexly intertwined, the clarification of these mechanisms may contribute to therapeutic strategies in SMARCB 1/ INI 1‐deficient tumors. In terms of pathological classifications, SMARCB 1/ INI 1‐deficient tumors may be re‐classified by genetic backgrounds.