Background. Increasing evidence argues that soluble CXCL16 promotes proliferation, migration, and invasion of cancer cells in vitro. However, the role of transmembrane or cellular CXCL16 in cancer remains relatively unknown. In this study, we determine the function of cellular CXCL16 as tumor suppressor in breast cancer cells. Methods. Expression of cellular CXCL16 in breast cancer cell lines was determined at both RNA and protein levels. In vitro and in vivo studies that overexpressed or downregulated CXCL16 were conducted in breast cancer cells. Results. We report differential expression of cellular CXCL16 in breast cancer cell lines that was negatively correlated with cell invasiveness and migration. Overexpression of CXCL16 in MDA-MB-231 cells led to a decrease in cell invasion and migration and induced apoptosis of the cells; downregulation of CXCL16 in MCF-7 cells increased cell migration and invasiveness. Consistent with the in vitro data, CXCL16 overexpression inhibited tumorigenesis in vivo. Conclusions. Cellular CXCL16 suppresses invasion and metastasis of breast cancer cells in vitro and inhibits tumorigenesis in vivo. Targeting of cellular CXCL16 expression is a potential therapeutic strategy for breast cancer.
Micro RNA s (mi RNA s) are confirmed to be tumor promoters or suppressors in multiple squamous cell carcinomas ( SCC s). miR‐99a‐5p has been demonstrated to be downregulated in cancerous tissues, but its functional role in head and neck SCC ( HNSCC ) and its mechanism of action have not been fully elucidated. Here, we studied the expression of miR‐99a‐5p in HNSCC and performed a clinical value assessment and then extracted mature expression data from The Cancer Genome Atlas ( TCGA ) and microarrays from Gene Expression Omnibus ( GEO ). Furthermore, biological analysis was constructed via online prediction tools. The results revealed that miR‐99a‐5p expression was markedly lower in HNSCC tissues than in normal tissues, which also showed significance in the prognosis of HNSCC . However, its diagnostic value could not be verified due to the lack of body fluid samples. Additionally, miR‐99a‐5p was expressed at higher levels in patients with low histological grade neoplasms than those with high histological grade neoplasms. The age of the patient might also be a possible clinical parameter affecting miR‐99a‐5p expression. Furthermore, miR‐99a‐5p significantly influenced HNSCC progression by regulating the PI 3K‐Akt signaling pathway, in which the key target genes were upregulated in 519 HNSCC tissues compared to 44 normal tissues, as determined by the Gene Expression Profiling Interactive Analysis ( GEPIA ). In conclusion, our study may provide insights into the expression and mechanism of miR‐99a‐5p in HNSCC . Further studies are required to elucidate the role of miR‐99a‐5p and its potential clinical applications for HNSCC .
BackgroundLung adenocarcinoma (LUAD) is the most frequent lung cancer. MicroRNAs (miRNAs) are believed to have fundamental roles in tumorigenesis of LUAD. Although miRNAs are broadly recognized in LUAD, the role of microRNA-375 in LUAD is still not fully elucidated.Material/MethodsWe evaluated the significance of miR-375 expression in LUAD by using analysis of a public dataset from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database and a literature review. Furthermore, we investigated the biological function of miR-375 by gene ontology enrichment and target prediction analysis.ResultsMiR-375 expression was significantly higher in LUAD by TCGA data compared to normal lung tissue (p<0.0001). In addition, a common pattern of upregulation for miR-375 in LUAD was found in our review of the literature. A total of 682 genes, both LUAD-related and miR-375-related, were obtained from the analytical integration. Critical pathways were unveiled in the network analysis of the overlaps, such as pentose and glucuronate interconversions, ascorbate and aldarate metabolism, and starch and sucrose metabolism. Furthermore, we identified covert miR-375 associated genes that might participate in LUAD by network analysis, such as FGF2 (fibroblast growth factor 2), PAX6 (paired box 6), and RHOJ. The expression of these three genes were all downregulated in LUAD. Finally, FGF2 was revealed to be negatively correlated with miR-375 in LUAD (r=−0.1821, p=0.0001).ConclusionsOverall, our study provides evidence that miR-375 is essential for the progression of LUAD.
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