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Updated: Mar 23, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

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TRIM65 negatively regulates p53 through ubiquitination

Yang Li1, Chengyuan Ma2, Tong Zhou3

  • 1Department of Respiration, The First Hospital of Jilin University, Changchun 130021, China.

Biochemical and Biophysical Research Communications
|March 26, 2016
PubMed

Insights

Tripartite-motif protein family member 65 (TRIM65) promotes non-small cell lung carcinoma (NSCLC) growth by degrading the tumor suppressor p53. Targeting TRIM65 may offer new NSCLC treatment strategies and overcome chemotherapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The role of Tripartite-motif protein family member 65 (TRIM65) in human cancer is not well understood.
  • TRIM65 is implicated in white matter lesions.
  • Non-small cell lung carcinoma (NSCLC) is a major human cancer with ongoing research into its molecular drivers.

Purpose of the Study:

  • To investigate the role of TRIM65 in the development and progression of non-small cell lung carcinoma (NSCLC).
  • To elucidate the molecular mechanisms by which TRIM65 influences cancer cell behavior.
  • To explore the potential of TRIM65 as a therapeutic target in NSCLC.

Main Methods:

  • Analysis of TRIM65 expression in NSCLC patient data using The Cancer Genome Atlas (TCGA).
  • Cell proliferation assays to assess the impact of TRIM65 overexpression and knockdown.
  • Co-immunoprecipitation and Western blotting to study TRIM65-p53 interaction and p53 degradation.
  • Experiments involving p53-positive and p53-negative cell lines to determine p53's role in TRIM65 function.

Main Results:

  • TRIM65 is significantly upregulated in a subset of NSCLC patients.
  • Overexpression of TRIM65 enhances NSCLC cell proliferation, while its knockdown inhibits it.
  • TRIM65 functions as an E3 ligase, targeting the tumor suppressor p53 for poly-ubiquitination and proteasomal degradation.
  • TRIM65 attenuates cisplatin-induced p53 activation and its inhibitory effect on cell growth is dependent on p53 status.

Conclusions:

  • TRIM65 acts as an oncogenic protein in NSCLC, likely by inactivating p53.
  • TRIM65 promotes tumor growth and may contribute to chemotherapy resistance.
  • Targeting TRIM65 presents a potential therapeutic strategy for NSCLC treatment.
Keywords:
NSCLCTRIM65Ubiquitinationp53

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