UCP2 promotes NSCLC proliferation and glycolysis via the mTOR/HIF-1α signaling

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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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Cailu Song1, Qing Liu1, Jing Qin2

  • 1State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.

Cancer Medicine
|January 13, 2024
PubMed
Abstract

Insights

Uncoupling protein 2 (UCP2) is upregulated in non-small cell lung cancer (NSCLC), promoting tumor growth and metabolic changes. Targeting the UCP2/mTOR/HIF-1α pathway offers a potential therapeutic strategy for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolism

Background:

  • Metabolic dysregulation is a key feature of cancer.
  • Uncoupling protein 2 (UCP2) is implicated in cancer malignancy and drug resistance.
  • The precise role of UCP2 in non-small cell lung cancer (NSCLC) tumor growth and metabolic reprogramming remains unclear.

Purpose of the Study:

  • To investigate the expression and function of UCP2 in NSCLC.
  • To elucidate the mechanism by which UCP2 influences NSCLC progression.
  • To explore the UCP2/mTOR/HIF-1α axis as a potential therapeutic target in NSCLC.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to assess UCP2 expression.
  • Functional assays including colony formation, CCK-8, and glycolysis assays to evaluate UCP2's impact on NSCLC cells.
  • Western blotting to confirm the regulatory mechanism of UCP2 on the mammalian target of rapamycin (mTOR) and hypoxia-inducible factor-1 alpha (HIF-1α) signaling pathways.

Main Results:

  • UCP2 expression was significantly elevated in NSCLC tissues and cell lines, correlating with poorer patient outcomes.
  • Downregulation of UCP2 suppressed NSCLC cell proliferation and glycolysis.
  • UCP2 was found to promote NSCLC tumorigenesis by regulating the mTOR/HIF-1α signaling axis.

Conclusions:

  • The study reveals the critical role of UCP2 in promoting NSCLC progression through the mTOR/HIF-1α pathway.
  • UCP2 acts as a potential biomarker for NSCLC prognosis.
  • The UCP2/mTOR/HIF-1α axis represents a promising therapeutic target for NSCLC treatment.
Keywords:
HIF-1αNSCLCUCP2glycolysismTORproliferation

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