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Updated: Sep 10, 2025

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Persistent lineage plasticity driving lung cancer development and progression.

Fanchen Meng1, Jianyu Li1, Zhijun Xia1

  • 1Department of Thoracic Surgery, Jiangsu Key Laboratory of Innovative Cancer Diagnosis & Therapeutics, Jiangsu Cancer Hospital & Nanjing Medical University Affiliated Cancer Hospital & Jiangsu Institute of Cancer Research, Nanjing, China.

Clinical and Translational Medicine
|August 23, 2025
PubMed
Summary

Lung cancer cells can change their identity, a process called lineage plasticity, which drives tumor progression and therapy resistance. Understanding this plasticity offers new targets for effective lung cancer treatments.

Keywords:
histopathologic transitionlineage imbalancelung cancerlung development

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Area of Science:

  • Oncology
  • Cell Biology
  • Genetics

Background:

  • Lung cancer exhibits significant heterogeneity across histologic types (adenocarcinoma, squamous, small-cell).
  • Tumor cells can shift between states, demonstrating lineage plasticity—the reprogramming of differentiated cells to alternate identities.
  • Genomic/epigenomic diversity and microenvironmental cues drive plasticity from disease onset.

Purpose of the Study:

  • To review the role of lineage plasticity in lung cancer progression, immune escape, and therapy resistance.
  • To integrate insights from normal lung development to understand how fate programs are co-opted in cancer.
  • To explore novel therapeutic strategies targeting lineage plasticity.

Main Methods:

  • Synthesized recent research findings on lung cancer lineage plasticity.
  • Integrated insights from lung tissue development.
  • Focused on transcriptional/epigenetic regulators and tumor microenvironmental factors.
  • Discussed the impact of EGFR and KRAS mutations.

Main Results:

  • Lineage plasticity is integral to lung cancer progression, from early tumorigenesis to metastasis and treatment resistance.
  • Lineage transitions are driven by genomic/epigenetic alterations and shaped by microenvironmental forces (hypoxia, stromal/immune cells).
  • Specific driver mutations may require lineage reprogramming for tumor initiation.

Conclusions:

  • Lineage plasticity provides a mechanistic framework linking lung cancer origin, evolution, and therapeutic vulnerabilities.
  • Understanding lineage plasticity is crucial for developing more effective lung cancer therapies.
  • Targeting lineage plasticity offers innovative therapeutic strategies.