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Blocking mutation independent p53 aggregation by emodin modulates autophagic cell death pathway in lung cancer

Ejazul Haque1, Mohd Kamil1, Safia Irfan1

  • 1Department of Biosciences, Faculty of Science, Integral University, Lucknow, 226026, India.

The International Journal of Biochemistry & Cell Biology
|January 23, 2018
PubMed

Insights

p53 protein aggregates can form even without TP53 mutation, as seen in wild-type A549 lung cancer cells. Inhibiting these aggregates with emodin boosts autophagy, potentially restoring p53 function in cancer cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Biology

Background:

  • Loss of p53 function due to mutation is a frequent cause of human cancers.
  • Recent studies suggest that self-aggregated p53 in cancer cells contributes to altered functions and cancer development.
  • The precise mechanism driving p53 self-aggregation, particularly concerning TP53 mutations, remains incompletely understood.

Purpose of the Study:

  • To investigate the differential aggregation patterns of p53 protein in cells with mutated TP53 versus wild-type TP53.
  • To explore the impact of inhibiting p53 protein aggregation on cellular processes like autophagy.
  • To elucidate the mechanistic link between p53 aggregation, autophagy, and potential restoration of p53 function.

Main Methods:

  • Comparative analysis of p53 aggregation in HaCaT keratinocytes (mutant TP53) and A549 lung cancer cells (wild-type TP53).
  • Treatment with emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) to inhibit p53 protein aggregation.
  • Assessment of autophagy levels and the role of ATG5 in p53 aggregation and dissociation.

Main Results:

  • p53 protein aggregates were observed in A549 cells with wild-type TP53, contrary to expectations.
  • Normal HaCaT keratinocytes with mutant TP53 did not exhibit p53 protein aggregates.
  • Emodin treatment inhibited p53 aggregation, significantly elevated autophagy in A549 cells, and caused dissociation of ATG5 from p53 aggregates.
  • Autophagy levels in HaCaT cells were not significantly affected by emodin treatment.

Conclusions:

  • p53 protein aggregation is not exclusively linked to TP53 mutation.
  • Inhibition of p53 aggregation by emodin induces autophagy in A549 lung cancer cells.
  • Increased autophagy may serve as a mechanism to remove p53 aggregates, potentially restoring p53 function in cancer cells.
Keywords:
A549 cell lineAutophagyEmodinHaCaT cell linep53 protein aggregation

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