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

Yeong Chang Chen, Meng Ya Chang, Ai-Li Shiau, Yi Te Yo, Chao-Liang Wu

Research output: Contribution to journalArticle

17 Citations (Scopus)

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 p21WAF1/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.

Original languageEnglish
Pages (from-to)981-990
Number of pages10
JournalJournal of Cellular Biochemistry
Volume100
Issue number4
DOIs
Publication statusPublished - 2007 Mar 1

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cell Biology

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