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Regulation of senescence and the SASP by the transcription factor C/EBP beta

  1. Author:
    Salotti,Jacqueline
    Johnson,Peter

  2. Author Address

    NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
    1. Year: 2019
    2. Date: Dec
    3. Epub Date: 2019 10 21
  2. Journal: Experimental gerontology
  3. PERGAMON-ELSEVIER SCIENCE LTD,
    1. 128
  5. Type of Article: Review
  6. Article Number: 110752
  7. ISSN: 0531-5565
  1. Abstract:

    Oncogene-induced senescence (OIS) serves as an important barrier to tumor progression in cells that have acquired activating mutations in RAS and other oncogenes. Senescent cells also produce a secretome known as the senescence-associated secretory phenotype (SASP) that includes pro-inflammatory cytokines and chemokines. SASP factors reinforce and propagate the senescence program and identify senescent cells to the immune system for clearance. The OIS program is executed by several transcriptional effectors that include p53, RB, NF-kappa B and C/EBP beta. In this review, we summarize the critical role of C/EBP beta in regulating OIS and the SASP. Post-translational modifications induced by oncogenic RAS signaling control C/EBP beta activity and dimerization, and these alterations switch C/EBP beta to a pro-senescence form during OIS. In addition, C/EBP beta is regulated by a unique 3'UTR-mediated mechanism that restrains its activity in tumor cells to facilitate senescence bypass and suppression of the SASP.

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External Sources

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  2. DOI: 10.1016/j.exger.2019.110752
  3. PMID: 31648009
  4. View record in Web of Science®
  5. WOS: 000498165000016

Library Notes

  1. Fiscal Year: FY2019-2020
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