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Original Research

Open Access

NR3C2 inhibits glycolysis in non-small cell lung cancer cells by regulating the Akt pathway

  • Yeqing Guo1,2,3
  • Yang Guo4
  • Xinyu Song1,2,3,*,

1Department of Respiratory and Critical Care Medicine, The first College of Clinical Medicine Science, China Three Gorges University, 443003 Yichang, Hubei, China

2Department of Respiratory and Critical Care Medicine, Yichang Central People’s Hospital, 443003 Yichang, Hubei, China

3Clinical Medical Research Center for Precision Diagnosis and Treatment of Lung Cancer and Management of Advanced Cancer Pain of Hubei Province, 443003 Yichang, Hubei, China

4Department of Pharmacy, Affiliated Renhe Hospital of China Three Gorges University, 443001 Yichang, Hubei, China

DOI: 10.22514/jomh.2025.075 Vol.21,Issue 5,May 2025 pp.130-136

Submitted: 31 March 2025 Accepted: 30 April 2025

Published: 30 May 2025

*Corresponding Author(s): Xinyu Song E-mail: songxinyu_1st@163.com

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Abstract

Background: Uncertainty surrounds the function of Nuclear Receptor Subfamily 3 Group C Member 2 (NR3C2) in controlling glycolysis in non-small cell lung cancer (NSCLC) and its molecular relationship to the Akt (Protein kinase B) pathway. In a number of malignancies, NR3C2 has been identified as a tumor suppressor. This research attempts to show how NR3C2 inhibits the development of NSCLC. Methods: The expression of NR3C2 and its impact on patient survival in NSCLC were investigated using a public database. Following NR3C2 overexpression via plasmid transfection, cell viability was assessed using Cell Counting Kit-8 (CCK8) assays. The colony formation assay was used to evaluate cell proliferation. Adenosine Triphosphate (ATP) generation, glucose uptake, and lactate production were measured in cells using appropriate kits. Cell apoptosis was assessed by flow cytometry. Western blotting was employed to evaluate protein expression levels of NR3C2, cleaved- Poly ADP-ribosepolymerase (PARP), cleaved-caspase3, Glucose transporter 1 (GLUT1), hexokinase2 (HK2), p-Akt/Akt and p-mammalian target of rapamycin (mTOR)/mTOR. Results: Database analysis revealed reduced NR3C2 expression in tumor. Overexpression of NR3C2 resulted in increased apoptosis and impaired colony formation and cell survival, and inhibited glucose consumption, lactate production and ATP levels. Furthermore, apoptotic indicators cleaved-PARP and cleaved-caspase3 showed markedly increased protein levels, whereas p-Akt/Akt, p-mTOR/mTOR, GLUT1 and HK2 showed markedly decreased levels. Conclusions: NR3C2 suppresses NSCLC cell proliferation and glycolysis, potentially through the suppression of the Akt pathway.


Keywords

NSCLC; NR3C2; Proliferation; Glycolysis; Apoptosis; Akt


Cite and Share

Yeqing Guo,Yang Guo,Xinyu Song. NR3C2 inhibits glycolysis in non-small cell lung cancer cells by regulating the Akt pathway. Journal of Men's Health. 2025. 21(5);130-136.

URL:

https://www.jomh.org/articles/10.22514/jomh.2025.075

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