The Inflammatory Chemokine CCL20 Modulates the Phosphorylation of Key Proteins in Stem Cell-Like Properties of Non-Small Cell Lung Cancer via the PI3K/AKT/mTOR Signaling Pathway

¹Department of Central Laboratory, Shanxi Province Cancer Hospital/ Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/ Cancer Hospital Affiliated to Shanxi Medical University, Shanxi 030000, China
²School of Medical Sciences, Shanxi Medical University, Taiyuan 030001, China
³Department of Neurosurgery, Shanxi Province Cancer Hospital/ Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/ Cancer Hospital Affiliated to Shanxi Medical University, Shanxi 030000, China

*Corresponding author: Lei Zhao, Department of Neurosurgery, Shanxi Province Cancer Hospital/ Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences/ Cancer Hospital Affiliated to Shanxi Medical University, Shanxi 030000, China Email: [email protected]

Received Date: August 27, 2026
Published Date: September 07, 2026

Citation: Du J, et al. (2026). The Inflammatory Chemokine CCL20 Modulates the Phosphorylation of Key Proteins in Stem Cell-Like Properties of Non-Small Cell Lung Cancer via the PI3K/AKT/mTOR Signaling Pathway. Mathews J Cancer Sci. 11(1):54

Copyrights: Du J, et al. © (2026).

ABSTRACT

Objective: Investigate the effect of CCL20 on the stem cell-like properties of non-small cell lung cancer and its mechanism.

Methods: By culturing A549 cells under serum-free conditions, to establish stem cell-like properties non-small cell lung cancer model. Using RT-qPCR and tube formation to validate the stemness characteristics of NSCLCSCs. The CCK-8 assay was used to determine cell viability, and the optimal concentration of CCL20 was determined. Western blotting was used to detect the phosphorylation levels of pathway proteins in response to CCL20, and the CCK8 assay was employed to assess the resistance to cisplatin and gefitinib following CCL20 treatment.

Results: NSCLCSCs treated with CCL20 exhibited increased stemness gene expression, PI3K, AKT, and mTOR phosphorylation levels were significantly elevated. The IC₅₀ values for Cisplatin and Gefitinib treated with CCL20 were significantly higher than those in the control group.

Conclusion: CCL20 significantly promotes stem cell-like characteristics in NSCLC cells, including enhancing self-renewal capacity, upregulating expression of stem cell markers, and increasing drug resistance. CCL20 regulates the stem cell-like characteristics of NSCLC through activation of the PI3K/AKT/mTOR signaling pathway. CCL20 holds promise as a novel therapeutic target for the treatment of NSCLC, offering new strategies for clinical management.

Keywords: CCL20, NSCLC, Drug Resistance, Stemness Markers, Western Bloating, PI3K/AKT/mTOR Signaling Pathway