Mitochondrial ribosomal protein S36 delays cell cycle progression in association with p53 modification and p21WAF1/CIP1 expression

被引:29
作者
Chen, Yeong-Chang
Chang, Meng-Ya
Shiau, Ai-Li
Yo, Yi-Te
Wu, Chao-Liang
机构
[1] Natl Cheng Kung Univ, Coll Med, Dept Biochem & Mol Biol, Tainan 701, Taiwan
[2] Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci, Tainan 701, Taiwan
[3] Natl Cheng Kung Univ, Coll Med, Dept Microbiol & Immunol, Tainan 701, Taiwan
关键词
mitochondrial ribosomal protein S36; p21(WAF1/CIP1) expression; p53; modification; cell cycle delay;
D O I
10.1002/jcb.21079
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ribosomal biogenesis is correlated with cell cycle, cell proliferation, cell growth and tumorigenesis. Some oncogenes and tumor suppressors are involved in regulating the formation of mature ribosome and affecting the ribosomal biogenesis. In previous studies, the mitochondrial ribosomal protein L41 was reported to be involved in cell proliferation regulating through p21(WAF1/CIP1) and p53 pathway. In this report, we have identified a mitochondrial ribosomal protein S36 (mMRPS36), which is localized in the mitochondria, and demonstrated that overexpression of mMRPS36 in cells retards the cell proliferation and delays cell cycle progression. In addition, the mMRPS36 overexpression induces p21(WAF1/CIP1) expression, and regulates the expression and phosphorylation of p53. Our result also indicate that overexpression of mMRPS36 affects the mitochondrial function. These results suggest that mMRPS36 plays an important role in mitochondrial ribosomal biogenesis, which may cause nucleolar stress, thereby leading to cell cycle delay.
引用
收藏
页码:981 / 990
页数:10
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