Gelsolin regulates proliferation, apoptosis, migration and invasion in human oral carcinoma cells

Abstract

Abstract. Gelsolin (GSN) is one of the most abundant actin-binding proteins, and is involved in several pathological processes, including Alzheimer's disease, cardiac injury and cancer. The aim of the present study was to assess the effect of GSN on the growth and motility of oral squamous cell carcinoma Tca8113 cells. The overexpression vector pcDNA3.1-GSN was transfected into Tca8113 cells and the stable GSN overexpression cell line was identified based on G418 antibiotic selection. The effect of GSN overexpression on the proliferation, apoptosis, migration and invasion of Tca8113 cells was examined using a cell counting kit-8 assay, flow cytometry and Transwell assays. The results revealed that GSN overexpression significantly promoted the cell proliferation and apoptosis of Tca8113 cells. In addition, Transwell assays demonstrated that the migration and invasion abilities of Tca8113 cells were enhanced by GSN overexpression. Therefore, the upregulation of GSN promotes cell growth and motility, indicating that it may perform a vital function in the progression of human oral cancers. IntroductionIn eukaryotic species, the actin cytoskeleton is essential for numerous cellular functions, including maintenance of morphology, motility, division, adhesion, endocytosis, intracellular transport and signal transduction (1-5). The varied and complex activities of the actin cytoskeleton are dynamically regulated by actin-binding proteins (ABPs) (2-4,6,7). Gelsolin (GSN) is one of the most abundant ABPs, and has been found to be a multifunctional regulator of physiological and pathological cellular processes (7,8).Previous studies have indicated that GSN may be a tumor suppressor that exerts a crucial role in the carcinogenic process (7,9). However, biphasic expression of GSN in oral precancerous lesions and oral cancers has been observed, which revealed a downregulation in GSN between oral precancerous lesions and oral cancers, and demonstrated upregulation of GSN in the stages of oral cancer progression (8). The biphasic expression indicated that GSN may perform a more complicated role in oral cancer biology.In order to study the biological roles in oral cancer development in the present study, GSN was overexpressed in oral cancer Tca8113 cells, and the effect of GSN on the proliferation, apoptosis, cell cycle, migration and invasion of these cells was investigated, which may contribute to the present understanding of the biological actions of GSN. Materials and methodsTca8113 cell culture. The human oral squamous cell carcinoma Tca8113 cell line was provided by the Shanghai Ninth People's Hospital, Medical School of Shanghai Jiao Tong University (Shanghai, China). The cells were cultured in RPMI 1640 medium (Gibco-BRL, Carlsbad, CA, USA) containing 10% fetal bovine serum (FBS), 100 µg/ml streptomycin and 100 units/ml penicillin, at 37˚C in a 5% CO 2 atmosphere.Stable transfection. To transiently transfect GSN into the Tca8113 cells, 0.5x10 5 cells/well were seeded into a 24-well plate (Corning, Inc., Corning, NY, USA)...

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