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p53 upregulates PLCε-IP3-Ca2+ pathway and inhibits autophagy through its target gene Rap2B

Jiehui Di1,2, Juanjuan Tang1,3, Heya Qian1

  • 1Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu, P.R. China.

Oncotarget
|October 15, 2017
PubMed

Insights

The tumor suppressor p53 regulates cell functions and inhibits autophagy by upregulating its target gene, Rap2B. This discovery offers a potential new strategy for cancer therapy.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The tumor suppressor p53 is crucial for regulating cellular processes including proliferation, metabolism, growth, and autophagy.
  • Identifying novel p53 target genes is essential for understanding its multifaceted roles in cellular regulation and disease.

Purpose of the Study:

  • To identify novel target genes of p53 using an unbiased approach.
  • To investigate the role of the identified gene, Rap2B, in p53-mediated cellular responses, particularly autophagy.

Main Methods:

  • Utilized an unbiased microarray approach to screen for novel p53 target genes.
  • Quantified intracellular levels of inositol trisphosphate (IP3) and calcium ions (Ca2+).
  • Measured levels of microtubule-associated protein 1A/1B-light chain 3 (LC3) protein to assess autophagy.

Main Results:

  • Identified Rap2B, a member of the Ras-related GTP-binding protein superfamily, as a novel p53 target gene with increased expression in human cancers.
  • Demonstrated that p53 upregulates Rap2B, leading to increased intracellular IP3 and Ca2+ levels.
  • Showed that p53, via Rap2B, decreases LC3 protein levels, indicating inhibition of autophagy.

Conclusions:

  • p53 inhibits starvation-induced autophagy through the Rap2B-Phospholipase C epsilon (PLCε)-IP3-Ca2+ pathway.
  • Rap2B is a confirmed target gene of p53 and plays a role in regulating autophagy.
  • Further research into Rap2B's functions in autophagy and tumorigenesis may yield novel cancer therapeutic strategies.

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