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June 27, 2026CellsOpen Access

c-MET Overexpression Drives AKT Activation, and Combined Inhibition Synergistically Enhances Therapeutic Sensitivity in Non-Small-Cell Lung Cancer

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Authors

PPPoyil PratheeshkumarRBRafia BegumSTSaravanan Thangavel

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Overview

Randomized trial evaluates c-MET and AKT targeting to improve therapeutic sensitivity in NSCLC, indicating a promising strategy.

Key Points

  • This study investigates the role of c-MET overexpression in AKT activation and its implications for therapy in non-small-cell lung cancer (NSCLC).
  • Analyzed c-MET and p-AKT expression using tissue microarray and TCGA datasets.
  • Conducted functional studies on NSCLC cell lines to assess the effects of pharmacological inhibition of c-MET and AKT.
  • Validated findings with in vivo experiments to measure tumor growth and toxicity.
  • c-MET overexpression correlated with higher p-AKT levels and poorer survival outcomes (log-rank p = 0.0223; HR = 1.234, 95% CI: 1.029–1.480).
  • Combined inhibition of c-MET and AKT significantly enhanced apoptosis and reduced cell viability compared to single agents.
  • In vivo combination therapy delayed tumor growth without significant toxicity.

Cite This Study

Pratheeshkumar et al. (2026) studied this question.

synapsesocial.com/papers/6a3f6972aea7db3c19540355https://doi.org/10.3390/cells15131155
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Prevalence, molecular characterization, and prognosis of c-Met protein overexpression in a real-world cohort of patients with non-squamous non-small cell lung cancer2025
  2. 2Abstract 11: Artificial intelligence-based spatial analysis of the local tumor microenvironment in relation to c-MET expression in non-small cell lung cancer.2026
  3. 3AXL and c‐Met Dual‐Targeting in Non‐Small Cell Lung Cancer: A Review of Small‐Molecule Inhibitors and Their Structure–Activity Relationships2026
  4. 4Clinical significance of c-Met expression in patients with advanced gastroesophageal adenocarcinoma.2026
  5. 5Abstract 6972: Programmed death-ligand 1 (PD-L1) upregulates c-MET phosphorylation via protein tyrosine phosphatase and contributes to the development of <i>MET</i> amplification in epidermal growth factor receptor (EGFR) mutant non-small cell lung cancer2024