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La influencia de CXCL9 en los macrófagos M2 en el desarrollo del cáncer de pulmón
Lin Mi1,2, Liyun Xu3, Zhijun Chen1
1Department of Cardiothoracic Surgery, Zhoushan Hospital, Zhoushan, China.
Background:
Lung cancer has the highest incidence among malignant tumors, and its high degree of metastasis and invasion, tendency to metastasis, and mortality rate are the key factors leading to treatment failure and poor prognosis. Tumor-associated macrophages (TAMs), which often exhibit an M2-polarized phenotype, are known to promote tumor progression. Notably, the chemokine CXCL9 has emerged as a critical regulator that can inhibit M2 macrophage polarization, thereby potentially suppressing tumor growth. This study combined clinical sample testing and prognostic analysis with cell behaviorology and molecular biology to systematically investigate the role and regulatory mechanism of CXCL9 in the tumor microenvironment of lung cancer.
Methods:
THP-1 cells were induced to differentiate into M1 and M2 macrophages. The effects of M2 macrophages on the proliferation, migration, and invasion of A549 lung adenocarcinoma cells were detected via Cell Counting Kit-8 cell viability, scratch-wound, and Transwell invasion assays. The effects of CXCL9 on M2 macrophage function and the expression of related proteins were detected via enzyme-linked immunosorbent assay, reverse transcription polymerase chain reaction, and Western blotting.
Results:
CXCL9 significantly inhibited the promoting effects of M2 macrophages on the proliferation, migration, metastasis and invasion of A549 cells. Specifically, CXCL9 inhibited M2 macrophage polarization by reducing the expression of surface markers CD16, CD32, and CD206. CXCL9 also inhibited the expression of VEGF-C, MMP9, and MMP2, thereby inhibiting tumor cell invasion and metastasis. Moreover, CXCL9 inhibited the activation of the ERK and AKT signaling pathways, further inhibiting tumor cell proliferation and invasion.
Conclusions:
CXCL9 inhibits the proliferation, migration, metastasis and invasion of lung cancer cells by inhibiting M2 macrophage polarization and function, indicating that CXCL9 may serve as a potential therapeutic target for lung cancer.
