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Proteomic identification of chaperonin-containing tail-less complex polypeptide-1 gamma subunit as a p53-responsive

Shao Chin Lee1, Jason Chan

  • 1National University Medical Institute, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. shaochinlee@yahoo.com

Cancer Genomics & Proteomics
|March 9, 2012
PubMed

Insights

Loss of p53 in colon cancer cells alters responses to drug treatment. This study identifies a novel signaling loop involving p53, TCP-1γ phosphorylation, and centrosome regulation in HCT116 cells.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cell signaling

Background:

  • Functional loss of p53 impacts human HCT116 colon cancer cell responses to apoptosis.
  • Understanding differential drug responses in cancer cells requires molecular investigation.

Purpose of the Study:

  • To compare protein expression between p53(+/+) and p53(-/-) HCT116 colon cancer cells.
  • To elucidate the molecular basis for altered drug responses in p53-deficient colon cancer.

Main Methods:

  • Proteomic analysis of HCT116 colon cancer cells with and without p53.
  • Identification and characterization of TCP-1γ protein variants.
  • Confirmation of tyrosine phosphorylation on TCP-1γ variants.

Main Results:

  • Two isoelectric variants of chaperonin-containing tail-less complex polypeptide-1 gamma subunit (TCP-1γ) were identified.
  • TCP-1γ variants were phosphorylated at tyrosine residue(s).
  • p53(-/-) cells exhibited higher concentrations of a more acidic TCP-1γ variant and TCP-1γ co-localized with centrosomes.

Conclusions:

  • A novel cell signaling loop involving p53 and TCP-1γ phosphorylation is implicated in HCT116 cells.
  • This pathway may regulate centrosome function and action in colon cancer.
  • Findings contribute to understanding p53's role in colon cancer cell signaling and drug response.

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