S100A16 promotes differentiation and contributes to a less aggressive tumor phenotype in oral squamous cell carcinoma.

摘要: Altered expression of S100A16 has been reported in human cancers, but its biological role tumorigenesis is not fully understood. This study aimed to investigate the clinical significance and functional oral squamous cell carcinoma (OSCC) suppression. mRNA and/or protein levels were examined by quantitative RT-PCR immunohistochemistry whole- laser microdissected-specimens normal mucosa (NHOM, n = 65), dysplastic lesions (ODL, n = 21), OSCCs (n = 132) positive cervical nodes (n = 17). OSCC was for correlations with clinicopathological variables patient survival. over-expressed knocked-down OSCC-derived (CaLH3 H357) cells employing retroviral constructs effects on proliferation, sphere formation three dimensional (3D)-organotypic invasive abilities vitro a mouse xenograft model. Both found be progressively down-regulated from NHOM ODL OSCC. Low significantly correlated reduced 10-year overall survival poor tumor differentiation. Analysis two external microarray datasets showed correlation between keratinocyte differentiation markers. CaLH3 H357 fractions enriched differentiated either lack adherence collagen IV or FACS sorting low p75NTR expressed higher than subpopulations less cells. Corroborating these findings, mediated over-expression knock-down led respective up- down-regulation In studies significant reduction 3D-invasive upon over-expression. These associated concomitant self-renewal (Bmi-1 Oct 4A) invasion related (MMP1 MMP9) molecules. also suppressed model resulting xenografts displayed features/expression increased proliferation/self-renewal. results indicate that promoting might function as suppressor