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SM22α inhibits cell proliferation and protects against anticancer drugs and γ‐radiation in HepG2 cells: Involvement of metallothioneins
Author(s) -
Kim Tae Rim,
Moon Ji Hye,
Lee Hee Min,
Cho Eun Wie,
Paik Sang Gi,
Kim In Gyu
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.09.040
Subject(s) - cytotoxic t cell , microbiology and biotechnology , cell growth , apoptosis , protein kinase b , metallothionein , chemistry , cell , mapk/erk pathway , biology , signal transduction , biochemistry , in vitro , gene
Smooth muscle protein 22‐alpha (SM22α) has been postulated to affect the structure and function of the actin filament. In this study, we report on the significant induction of SM22α by cytotoxic agents in HepG2 cells. SM22α‐overexpression inhibited the activation of IGF‐1Rβ/Akt and Erk, consequently suppressing cell proliferation. On the other hand, SM22α‐overexpressing cells became resistant to apoptotic cell death caused by cytotoxic agents, in which metallothionein (MT) isoforms, especially MT1G, were significantly induced. MT1G‐overexpression also conferred cellular resistance, and SM22α regulated the expression of MT1G at a transcriptional level. This study provides the first demonstration of SM22α‐induced blockage of cell proliferation and cellular resistance to overcome the detrimental effects of damaging agents.