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PML: Regulation and multifaceted function beyond tumor suppression

  1. Author:
    Hsu, Kuo-Sheng
    Kao, Hung-Ying

  2. Author Address

    Case Western Reserve Univ, Dept Biochem, 10900 Euclid Ave, Cleveland, OH 44106 USA.Case Western Reserve Univ, Comprehens Canc Ctr, Cleveland, OH 44106 USA.Univ Hosp Cleveland, Cleveland, OH 44106 USA.NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA.
    1. Year: 2018
    2. Date: Jan 25
  2. Journal: Cell and Bioscience
  3. BIOMED CENTRAL LTD,
    1. 8
    2. Pages: 5
  5. Type of Article: Article
  6. Article Number: ARTN 5
  7. ISSN: 2045-3701
  1. Abstract:

    Promyelocytic leukemia protein (PML) was originally identified as a fusion partner of retinoic acid receptor alpha in acute promyelocytic leukemia patients with the (15; 17) chromosomal translocation, giving rise to PML-RARa and RAR alpha-PML fusion proteins. A body of evidence indicated that PML possesses tumor suppressing activity by regulating apoptosis, cell cycle, senescence and DNA damage responses. PML is enriched in discrete nuclear substructures in mammalian cells with 0.2-1 mu m diameter in size, referred to as alternately Kremer bodies, nuclear domain 10, PML oncogenic domains or PML nuclear bodies (NBs). Dysregulation of PML NB formation results in altered transcriptional regulation, protein modification, apoptosis and cellular senescence. In addition to PML NBs, PML is also present in nucleoplasm and cytoplasmic compartments, including the endoplasmic reticulum and mitochondria-associated membranes. The role of PML in tumor suppression has been extensively studied but increasing evidence indicates that PML also plays versatile roles in stem cell renewal, metabolism, inflammatory responses, neural function, mammary development and angiogenesis. In this review, we will briefly describe the known PML regulation and function and include new findings.

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External Sources

  1. View Full Text
  2. DOI: 10.1186/s13578-018-0204-8
  3. PMID: 29416846
  4. PMCID: PMC5785837
  5. View record in Web of Science®
  6. WOS: 000423374100001

Library Notes

  1. Fiscal Year: FY2017-2018
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