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Journal of Chinese Pharmaceutical Sciences ›› 2024, Vol. 33 ›› Issue (5): 430-437.DOI: 10.5246/jcps.2024.05.032

• Original articles • Previous Articles     Next Articles

Deciphering the mechanism of miR-128a-mediated proliferation of non-small cell lung cancer cells via phosphofructokinase and glycolysis

Xiang Zhang*(), Junlei Ying, Jiangwei Ni   

  1. Thoracic Surgery Department, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China
  • Received:2023-11-14 Revised:2024-01-26 Accepted:2024-02-16 Online:2024-05-31 Published:2024-05-31
  • Contact: Xiang Zhang
  • Supported by:
    Wenzhou Science and Technology Bureau Science and Technology Plan Basic Research Project (Grant No. Y20190443).

Abstract:

This study investigated the mechanism by which miR-128a, mediated through phosphofructokinase (PFK), fostered proliferation in non-small cell lung cancer (NSCLC) via glycolysis. Bioinformatics analysis was employed to predict microRNAs (miRNAs) involved in the interaction with PFK. Subsequently, the expression levels of the identified molecule were validated using qRT-PCR in both tumor tissues and cell samples. The modulation of this molecule’s expression was executed, and techniques such as immunofluorescence and Western blotting analysis were employed to evaluate apoptosis levels, PFK expression, and hypoxia-inducible factor-1 alpha (HIF1-α) expression in lung cancer cells. The results indicated that bioinformatics analysis revealed miR-128a as a potential targeting molecule for PFK. The expression level of miR-128a was significantly diminished in lung cancer cells. Overexpression of miR-128a led to increased apoptosis and reduced protein expression levels of PFK and HIF1-α. Conversely, decreased expression of miR-128a in lung cancer cells promoted cell proliferation by downregulating PFK and HIF1-α expression levels.

Key words: Non-small cell lung cancer, miR-128a, Phosphofructokinase, Proliferation

Supporting: