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Regulation of tubular recycling endosome biogenesis by the p53-MICALL1 pathway

Yukie Takahashi1, Chizu Tanikawa1, Takafumi Miyamoto1

  • 1Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

International Journal of Oncology
|July 18, 2017
PubMed

Insights

The tumor suppressor p53 regulates colorectal cancer cell development by controlling MICALL1 expression. This study reveals p53

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The p53 gene is frequently mutated in colorectal cancer, impacting tumor suppression.
  • Understanding the p53 downstream pathway is crucial for colorectal cancer treatment.

Purpose of the Study:

  • To comprehensively analyze the p53 downstream pathway in colorectal cancer using multi-omics data.
  • To identify novel p53 targets and their role in colorectal cancer development.

Main Methods:

  • Multi-omics analysis including mass spectrometry and TCGA database.
  • Screening of HCT116 p53+/+ and HCT116 p53-/- cells treated with adriamycin.
  • Analysis of gene expression and protein localization via siRNA inhibition.

Main Results:

  • Identified 124 proteins upregulated by DNA damage in a p53-dependent manner.
  • Discovered MICALL1 as a novel p53 target with functional binding sites.
  • Found decreased MICALL1 expression in p53-mutated colorectal cancer tissues.
  • Demonstrated p53-dependent co-localization of MICALL1, RAB8A, and CD2AP at tubular recycling endosomes.

Conclusions:

  • p53 transcriptionally regulates MICALL1, impacting tubular recycling endosome biogenesis.
  • MICALL1 expression is frequently suppressed in colorectal cancer, particularly in tumors with p53 mutations.
  • These findings highlight a novel p53-MICALL1 axis in colorectal cancer pathogenesis.

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