Scholarlink

<p>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 (<i>SFTPD</i>) expression is reduced to near absence in metastatic non-small cell lung cancer (NSCLC) tissue, linking its loss to metastatic progression. <i>SFTPD</i> 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 <i>SFTPD</i> expression is associated with reduced IL-4/STAT6 signaling, and patients with low <i>SFTPD</i> 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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Pulmonary surfactant protein D reduces lung cancer progression associated with decreased IL-4/STAT6 signaling

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月8日

查看全文
  • Ali Mohammadi,
  • Mohammed Inayatullah,
  • Anders Schlosser,
  • Bartosz Pilecki,
  • Niels Marcussen,
  • Seyda Ünsal,
  • Behzad Mansoori,
  • Behzad Baradaran,
  • Yousef Tallouzi,
  • Morten Frier Gjerstorff,
  • Jonas Graversen,
  • Kim Ravnskjær,
  • Vijay K. Tiwari,
  • Mikkel G. Terp,
  • Grith Lykke Sorensen

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.