Abstract
Problem The expression of KAI1 (a metastatic suppressor gene) in cancer cells results in reduced cell motility and invasiveness. A cDNA clone of VANGL1, a member of the tetraspanin protein family that specifically interacts with the COOH-terminal cytoplasm domain of KAI1, was isolated and renamed KITENIN (KAI1 COOH-terminal interacting tetraspanin). The purpose of this study was to investigate the role of KITENIN on the progression and metastasis of transfected squamous cell carcinoma using in vivo and in vitro experiments. Methods Locally advanced squamous cell carcinoma tissues from five patients were obtained for investigation of KITENIN expression. Malignant tumors, normal adjacent mucosa tissues, metastatic lymph nodes, and non-metastatic lymph nodes were collected. KITENIN or vector only (control) was transfected into SCC (squamous cell carcinoma) VII, a mouse squamous cell carcinoma cell line, using FuGENE 6. An in vitro assay (invasion, migration, and proliferation) for KITENIN and the vector-transfected group was studied. The KITENIN or vector-transfected SCC VII cells were injected subcutaneously into 12 C3H/HeJ syngeneic mice (6 mice for each group). The tumor size was measured daily for 4 weeks. During the fifth week after injection, the presence of metastasis in the lung and liver tissue was evaluated for each mouse with a tumor mass on the back; the tissues were assessed by gross and microscopic examination. Results KITENIN was highly expressed in tumors and metastatic lymph nodes from patients. KITENIN-transfected cells showed significantly increased invasion, migration, and proliferation compared with the vector-transfected cells. Tumor volume was more increased in the KITENIN-transfected cells-injected mice. Lung metastasis was found in the KITENIN-group (3/6 mice), while no metastasis in the vector-group. Conclusion KITENIN participates in the progression and metastasis of SCC. Significance An antisense KITENIN strategy may be a useful method to inhibit progression and metastasis in squamous cell carcinoma. Support This study was financially supported by Chonnam National University, 2006.
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