Thoracic cancer · 2026
Cigarette Smoke Extract Promotes Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer by Upregulating PRMT6.
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Zhang Yanwen, Chang Xiaojing, Cao Jie, Zhang Jing, Zhao Haiyan
Аннотация
BACKGROUND AND OBJECTIVE: Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide. Cigarette smoke extract (CSE) is a major environmental factor driving NSCLC progression, yet the underlying molecular mechanisms remain incompletely understood. Protein arginine methyltransferase 6 (PRMT6) is implicated in various malignancies, including NSCLC, and epithelial-mesenchymal transition (EMT) contributes to metastasis and poor prognosis in this disease. However, the role of PRMT6 in CSE-induced NSCLC progression has not been elucidated.
METHODS: NSCLC progression under CSE exposure was assessed using a subcutaneous xenograft model in nude mice and in vitro assays in H1299 cells. Tumor growth and molecular alterations were evaluated by immunohistochemistry, CCK-8, wound healing, Transwell, immunofluorescence, qRT-PCR, and western blotting.
RESULTS: CSE exposure enhanced H1299 cell proliferation, migration, and invasion in vitro and promoted xenograft tumor growth in vivo. This was accompanied by upregulated expression of PRMT6 and its effector H3R2me2a, elevated mesenchymal markers (N-cadherin, MMP2, MMP9, vimentin), and transcription factors (Snail, TWIST1), and increased phosphorylation of PI3K p85, Akt, and mTOR. Notably, all CSE-induced effects were abrogated by the PRMT6 inhibitor EPZ020411.
CONCLUSION: CSE promotes NSCLC progression by upregulating PRMT6, leading to PI3K/Akt/mTOR activation and EMT induction. These findings highlight PRMT6 as a potential therapeutic target in NSCLC.
METHODS: NSCLC progression under CSE exposure was assessed using a subcutaneous xenograft model in nude mice and in vitro assays in H1299 cells. Tumor growth and molecular alterations were evaluated by immunohistochemistry, CCK-8, wound healing, Transwell, immunofluorescence, qRT-PCR, and western blotting.
RESULTS: CSE exposure enhanced H1299 cell proliferation, migration, and invasion in vitro and promoted xenograft tumor growth in vivo. This was accompanied by upregulated expression of PRMT6 and its effector H3R2me2a, elevated mesenchymal markers (N-cadherin, MMP2, MMP9, vimentin), and transcription factors (Snail, TWIST1), and increased phosphorylation of PI3K p85, Akt, and mTOR. Notably, all CSE-induced effects were abrogated by the PRMT6 inhibitor EPZ020411.
CONCLUSION: CSE promotes NSCLC progression by upregulating PRMT6, leading to PI3K/Akt/mTOR activation and EMT induction. These findings highlight PRMT6 as a potential therapeutic target in NSCLC.