表面活性蛋白D
肺癌
癌症研究
腺癌
转移
肺
医学
信号转导
肿瘤进展
免疫系统
先天免疫系统
A549电池
表面活性蛋白A
下调和上调
癌症
临床意义
呼吸道疾病
细胞信号
免疫疗法
细胞
免疫学
生物
癌细胞
NFKB1型
PD-L1
基因表达
肿瘤发生
肺癌的治疗
作者
Ali Mohammadi,MOHAMMED INAYATULLAH,Anders Schlosser,Bartosz Pilecki,Niels Marcussen,Şeyda Ünsal,Behzad Mansoori,Behzad Baradaran,Yousef Tallouzi,Morten F. Gjerstorff,Jonas Heilskov Graversen,Kim Ravnskjær,Vijay Tiwari,Mikkel G. Terp,Lykke Sorensen Grith
标识
DOI:10.1038/s41698-025-01163-6
摘要
Pulmonary surfactant protein D (SP-D) is an innate immune molecule implicated in lung cancer, where its expression correlates with improved survival and reduced tumor growth. Despite its relevance to lung pathobiology, the transcriptional programs regulated by SP-D and their role in cancer progression and metastasis remain poorly understood. Through integrative analysis of multimodal human data we demonstrate that the SP-D gene (SFTPD) expression is reduced to near absence in metastatic non-small cell lung cancer (NSCLC) tissue, linking its loss to metastatic progression. SFTPD overexpression in A549 lung adenocarcinoma cells significantly decreased tumor growth and metastasis in vivo, and intranasal SP-D protein administration reduced lung tumor burden. Mechanistically, SP-D suppressed several signaling pathways, including IL-4/STAT6 signaling. Analysis of clinical lung tumor samples confirmed that SFTPD expression is associated with reduced IL-4/STAT6 signaling, and patients with low SFTPD expression and elevated IL-4 signaling in their tumors showed the poorest disease-free survival. Our findings demonstrate that SP-D interacts with NSCLC cells to suppress lung cancer progression, in part by blocking of the IL-4/STAT6 signaling pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI