Abstract
Abstract Members of multifunctional S100 protein family have been reported to be differentially expressed in a variety of human cancers and are functionally linked with various aspects of carcinogenesis. S100A14 is a recently identified member of the S100 protein family. Despite reports of altered expression in different cancer types, functional significance of S100A14 in carcinogenesis is largely unknown. In this study, we aimed to investigate the functional role of S100A14 proliferation and invasion of oral squamous cell carcinoma (OSCC)-derived cell. S100A14 mRNA and protein levels were found to be down-regulated in OSCCs and OSCC-derived cells compared to the corresponding normal controls. In addition, membranous S100A14 immunoexpression was found to be gradually lost in the invasive fronts/islands compared to the central/superficial part of OSCCs. Over-expression of S100A14, by using retroviral expression construct, was found to be associated with the inhibition of cell proliferation, induction of G1-arrest and up-regulation of p21 in OSCC-derived cell lines (CaLH3 and OSCC1) with wild type p53. Similarly, over-expression of S100A14 was associated with inhibition of invasive potential of OSCC-derived cells in the in vitro Matrigel invasion assay. S100A14 mediated inhibition of cellular invasion was found to be associated with modulation of mRNA signature of genes involved in tumor invasion and metastasis, in particular MMP1, MMP9. Taken together, these data suggest that similar to other multifunctional S100 protein members, S100A14 might be involved in OSCC progression by regulating cell proliferation and invasion. Hence, further characterization of the molecular pathways/targets of S100A14 might lead to the better understanding of proliferation and invasion of OSCC and this process, in future, might be useful as a diagnostic or therapeutic approach in cancers. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 24. doi:1538-7445.AM2012-24
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