Association of surfactant protein D with pulmonary metastases from colon cancer
Yuki Tajima, Masashi Tsuruta, Hirotoshi Hasegawa, Koji Okabayashi, Takashi Ishida, Masashi Yahagi, Akitsugu Makino, Kaoru Koishikawa, Shingo Akimoto, Don D. Sin, Yuko Kitagawa
Abstract
Surfactant protein D (SP‑D) is a member of the collectin family of proteins, which is secreted by airway epithelial cells. SP‑D serves an important role in the immune system and in the inflammatory regulation of the lung. SP‑D was recently found to suppress lung cancer progression by downregulating epidermal growth factor signaling. However, the relationship between SP‑D and pulmonary metastases from colon cancer remains unknown. The present study aimed to determine whether SP‑D may suppress the development of the mouse rectal carcinoma cell line, CMT93, <em>in vitro</em>. The present study investigated the effect of SP‑D on pulmonary metastases from colon cancer <em>in vivo</em> using SP‑D knockout mice. A wound healing assay and cell invasion assay revealed that SP‑D suppressed the proliferation, migration and invasion of CMT‑93 cells. After injection of CMT‑93 cells into the tail vein, SP‑D knockout mice were significantly more susceptible to developing pulmonary metastases than C57/BL6 mice (control). Moreover, a novel cell line (CMT‑93 pulmonary metastasis; CMT‑93 PM) was established from the lesions of pulmonary metastases in C57/BL6 mice following injection of CMT93 into the tail vein. CMT‑93 PM exhibited more robust invasion and proliferation compared to CMT93, which was unaffected by exposure to SP‑D. A higher incidence of pulmonary metastases was detected following injection of CMT93 PM into the tail vein of C57/BL6 mice compared with CMT‑93. Consequently, SP‑D may be involved in the pathogenesis of pulmonary metastases from colon cancer.