[No authors listed]
BACKGROUND:In this study, we investigated the role of artemin, a member of the glial cell-derived neurotrophic factor of ligands, in the malignant phenotype of lung cancer. METHODS:Artemin expression was examined in various types of lung cancer and normal lung tissues, as well as in lung cancer cell lines by immunohistochemistry and semi-quantitative PCR. Functional studies were performed using artemin overexpression or knockdown vectors in lung cancer cell lines. Methyl thiazolyl tetrazolium, flow cytometry, wound healing, and transwell assays were conducted to evaluate the contribution of artemin on tumor cell proliferation, migration, and invasion. RESULTS:Artemin is broadly expressed in lung cancer tissues, and is associated with tumor staging. Overexpression of artemin in NL9980 large cell lung cancer cells increased proliferating cells and enhanced migrating capability in wound healing and transwell assays, as well as demonstrating enhanced invasion capability. Silencing artemin in LTEP-α-2 adenocarcinoma cell lines decreased cellular proliferation, migration, and invasion capabilities. CONCLUSION:Artemin could promote the proliferation and invasiveness of lung cancer cells in vitro and therefore could be a new potential target to combat lung cancer.
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