Open Access

ARTICLE

ARPC1A Promotes NSCLC Malignancy via Stimulating the Drug Resistance and Cell Migration

Hongjuan Guo¹, Dan Liu^1,2, Ruyu Yan^1,2, Tianjing Zhang³, Kecheng Zhou^1,2,*, Minxia Liu^1,*

1 School of Life Sciences, Anhui Medical University, Hefei, 230032, China
2 Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China
3 Department of Orthopaedics, Hejin Shengji Hospital, Yuncheng, 043300, China

* Corresponding Authors: Kecheng Zhou. Email: ; Minxia Liu. Email:

BIOCELL 2025, 49(3), 483-502. https://doi.org/10.32604/biocell.2025.062143

Received 11 December 2024; Accepted 10 March 2025; Issue published 31 March 2025

Abstract

Objectives: Non-small cell lung cancer (NSCLC) represents a formidable malignancy characterized by its marked metastatic potential and intrinsic resistance to therapeutic interventions. The identification of potential biomarkers delineating the progression and metastatic cascade of NSCLC assumes paramount importance in fostering advancements toward enhanced patient outcomes and prognostic stratification. Methods: The expression level of the actin-related protein 2/3 complex; subunit 1A (ARPC1A) in NSCLC was evaluated using The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) databases; along with the LinkedOmics database for co-expression genes. Further verification of ARPC1A expression in normal lung cells and NSCLC cells; as well as in normal tissues and lung cancer tissues; was performed using quantitative real-time reverse transcription PCR (RT-qPCR) and Western blotting. The function of ARPC1A was explored through Gene Set Enrichment Analysis (GSEA) and immune infiltration analysis; followed by functional experiments for validation. Results: ARPC1A is upregulated in NSCLC and is associated with unfavorable clinical prognoses. Additionally, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis highlights a potential link between the ARPC1A gene and the cell cycle and p53 signaling pathways. ARPC1A also promotes cell proliferation and resistance to chemotherapeutic drugs, thereby enhancing the oncogenic potential of NSCLC. Relevant cell-based experiments confirm that targeted inhibition of ARPC1A effectively suppresses cellular migratory and invasive capabilities. The immune infiltration analysis showed a close association between ARPC1A expression and various immune components, suggesting ARPC1A may interact with the tumor microenvironment. Mechanistically, ARPC1A promotes cell migration by stimulating the epithelial-to-mesenchymal transition (EMT). Conclusion: The study results revealed the potential of ARPC1A as a valuable prognostic biomarker for NSCLC. Additionally, the associated mechanisms provide insights that may pave the way for therapeutic interventions for NSCLC patients.

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Supplementary Material

Supplementary Material File

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