4.7 Review

An emerging role of PARK2 in cancer

Journal

JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 92, Issue 1, Pages 31-42

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s00109-013-1107-0

Keywords

PARK2; Mutation; Deletion; Tumor suppressor; Mitophagy; Metabolism

Funding

  1. Singapore Ministry of Health's National Medical Research Council (NMRC) under its Singapore Translational Research (STaR) Investigator Award
  2. NMRC [NMRC/1311/2011]
  3. NIH [R01CA026038-23]
  4. Natural Science Foundation of China [81071788, 81272956]
  5. NATIONAL CANCER INSTITUTE [R01CA026038] Funding Source: NIH RePORTER

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PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer.

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