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CircPTK2 enhances non-small cell lung cancer proliferation by inhibiting cellular senescence through stabilizing NFYA

Qiuhui Li1,2,3, Kun Zhao4, Yili Shen1,2

  • 1Department of Respiratory Medicine, Huzhou Central Hospital, Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Huzhou, China.

British Journal of Pharmacology
|November 8, 2025
PubMed
Abstract

Insights

High circPTK2 expression in non-small cell lung cancer (NSCLC) promotes tumor growth by inhibiting cellular senescence. circPTK2 targets NFYA degradation, upregulating FOXM1 and worsening patient prognosis, suggesting circPTK2 as a therapeutic target.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Cellular senescence is a crucial factor in cancer development.
  • Circular RNAs (circRNAs) are implicated in various diseases, including cancer.
  • The specific role of circPTK2 in non-small cell lung cancer (NSCLC) remains unclear.

Purpose of the Study:

  • To investigate the role and underlying mechanism of circPTK2 in NSCLC.
  • To determine the relationship between circPTK2 expression and patient prognosis.
  • To explore circPTK2 as a potential therapeutic target for NSCLC.

Main Methods:

  • Lentivirus-mediated gene manipulation (knockdown/overexpression) to study circPTK2 effects on proliferation and senescence.
  • Tissue microarrays and in situ hybridization to analyze circPTK2 expression in NSCLC tissues.
  • RNA sequencing (RNA-seq) to identify circPTK2-regulated pathways and targets.
  • Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays to investigate transcriptional regulation.
  • Co-immunoprecipitation (Co-IP) to assess protein interactions and ubiquitination.

Main Results:

  • circPTK2 is highly expressed in NSCLC tissues and correlates with poor prognosis.
  • Knockdown of circPTK2 inhibits cancer cell growth and promotes cellular senescence.
  • circPTK2 binds to MDM2, preventing NFYA degradation and leading to FOXM1 upregulation.
  • NFYA directly regulates FOXM1, suppressing cellular senescence in NSCLC.

Conclusions:

  • Elevated circPTK2 expression is a marker of poor survival in NSCLC patients.
  • circPTK2 promotes NSCLC progression by inhibiting senescence through the NFYA/FOXM1 axis.
  • circPTK2 represents a promising therapeutic target for NSCLC treatment.
Keywords:
FOXM1MDM2NFYAcell proliferationcell senescencecircPTK2

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