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

✍ Scribed by Yeong-Chang Chen; Meng-Ya Chang; Ai-Li Shiau; Yi-Te Yo; Chao-Liang Wu

Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
275 KB
Volume
100
Category
Article
ISSN
0730-2312

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✦ Synopsis

Abstract

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. J. Cell. Biochem. 100: 981–990, 2007. © 2006 Wiley‐Liss, Inc.

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