Related Experiment Video

Updated: Jul 4, 2025

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

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TRIM34 suppresses non-small-cell lung carcinoma via inducing mTORC1-dependent glucose utilization and promoting

Pengfei Zhang1, Zhida Chen2, Juan Li3

  • 1Chinese PLA Medical School, Beijing, 100853, China; Department of Oncology, First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.

Archives of Biochemistry and Biophysics
|February 9, 2024
PubMed

Insights

The study found that TRIM34, a protein, suppresses non-small-cell lung carcinoma (NSCLC) progression by damaging mitochondria and promoting cell death. Lower TRIM34 levels correlate with NSCLC, suggesting its potential as a therapeutic biomarker.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Non-small-cell lung carcinoma (NSCLC) is a leading cause of cancer mortality.
  • The role of TRIM34 in NSCLC pathogenesis was previously uninvestigated.
  • TRIM34 is known to influence apoptosis and inflammation.

Purpose of the Study:

  • To investigate the regulatory role of TRIM34 in NSCLC.
  • To determine the molecular mechanisms underlying TRIM34's effects in NSCLC.

Main Methods:

  • Analysis of TRIM34 expression levels in NSCLC tissues.
  • In vitro and in vivo experiments assessing the impact of TRIM34 overexpression on NSCLC cells.
  • Utilizing rapamycin, an mTORC1 inhibitor, to investigate pathway involvement.

Main Results:

  • TRIM34 expression was found to be downregulated in NSCLC.
  • TRIM34 overexpression induced mitochondrial damage and apoptosis in NSCLC cells.
  • TRIM34 activated mTORC1 signaling, leading to accelerated glycolysis and suppressed tumor progression.
  • Rapamycin treatment reversed the effects of TRIM34 overexpression on mitochondrial damage and apoptosis.

Conclusions:

  • TRIM34 acts as a tumor suppressor in NSCLC by activating mTORC1-dependent glucose metabolism and promoting cell death.
  • TRIM34 holds potential as a therapeutic biomarker for NSCLC patients.
Keywords:
Cell apoptosisGlucose utilizationNSCLCTRIM34mTORC1

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