Polo-like kinases mediate cell survival in mitochondrial dysfunction

Takumi Matsumoto, Ping Yuan Wang, Wenzhe Ma, Joong Sung Ho, Satoaki Matoba, Paul M. Hwang

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Cancer cells often display defects in mitochondrial respiration, thus the identification of pathways that promote cell survival under this metabolic state may have therapeutic implications. Here, we report that the targeted ablation of mitochondrial respiration markedly increases expression of Polo-like kinase 2 (PLK2) and that it is required for the in vitro growth of these nonrespiring cells. Furthermore, we identify PLK2 as a kinase that phosphorylates Ser-137 of PLK1, which is sufficient to mediate this survival signal. In vivo, knockdown of PLK2 in an isogenic human cell line with a modest defect in mitochondrial respiration eliminates xenograft formation, indicating that PLK2 activity is necessary for growth of cells with compromised respiration. Our findings delineate a mitochondrial dysfunction responsive cell cycle pathway critical for determining cancer cell outcome.

Original languageEnglish (US)
Pages (from-to)14542-14546
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number34
StatePublished - Aug 25 2009
Externally publishedYes


  • Cell cycle
  • Respiration
  • sco2

ASJC Scopus subject areas

  • General


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