[Expression and significance of fibroblast growth factor receptor 2 in clear cell renal cell carcinoma].

OBJECTIVE: To investigate the expression of fibroblast growth factor receptor 2 (FGFR2) in clear cell renal cell carcinoma (ccRCC; or kidney renal clear cell carcinoma, KIRC), to analyze the relationship between the expression of FGFR2 and the clinical pathological features and prognosis of ccRCC, to study the relationship between the expression of FGFR2 and other molecules, and to explore its role in the development of ccRCC. METHODS: Gene expressional and clinical information of ccRCC patients were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus(GEO) database. Next, the data were transformed and collated. In the study, 104 clinical ccRCC samples and corresponding paracancerous normal tissue samples were collected from Department of Urology, Peking University First Hospital. Immunohistochemistry (IHC) was performed and the staining results were scored, so as to compare the expression of FGFR2 in ccRCC and paracancerous normal tissues. Besides, quantify real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression level of FGFR2 in normal renal epithelial cell lines (293) and ccRCC cell lines (786-O, 769-P, OSRC-2, Caki-1, ACHN, and A498). In addition, the relationship between FGFR2 expression and clinical pathological characteristics (including TNM staging and pathological grading) and survival prognosis in ccRCC patients was further analyzed. Furthermore, the relationship between FGFR2 expression and B cells, T cells, natural killer (NK) cells and neutrophil infiltration in the ccRCC patients was analyzed, and the Biological General Repository for Interactionh Datasets (BioGRID) was used to builds protein-protein interaction (PPI) networks to study molecules that interacted with the FGFR2 protein. RESULTS: In the TCGA database, the expression of FGFR2 was down-regulated in ccRCC tissue samples compared with normal tissue samples, and the expression in the GEO database also showed this differences. Furthermore, FGFR2 expression was downregulated in ccRCC clinical samples and ccRCC cell lines, compared with corresponding paracancerous normal tissue or normal renal epithelial cell lines. In addition, FGFR2 high expression was associated with earlier, lower-level ccRCC and was associated with a better prognosis in the patients with ccRCC. Moreover, FGFR2 expression was not significantly related to B cells, T cells, NK cells and neutrophil infiltration, and the PPI network showed that FGFR2 protein interacted with certain molecules. CONCLUSION: Our work sheds light on the potential role of FGFR2 in the development of ccRCC, suggesting that FGFR2 may serve as a prognostic marker and potential therapeutic target for patients with ccRCC.

[Inflammatory priming adipose derived stem cells significantly inhibit the proliferation of peripheral blood mononuclear cells].

OBJECTIVE: To explored whether adipose derived stem cells (ASCs) could inhibit the pro-liferation of peripheral blood mononuclear cells (PBMCs) and whether inflammatory priming could enhance this property of ASCs. METHODS: We isolated ASCs using collagenase from adipose tissue and expanded them in vitro. Cells were induced to differentiate into adipogenic and osteogenic lineages. The cells at passage 3 to passage 5 were used for the experiments. After carboxy fluoresce in succinimidyl ester (CFSE) staining, PBMCs were co-cultured with inflammatory priming ASCs. The PBMCs cultured without ASCs or with non-treated ASCs defined as control groups. Then we used flow cytometry to detect the proliferation of PBMCs. RESULTS: ASCs had fibroblast-like phenotype and were spindle shaped. They were able to differentiate into cells of adipogenic and osteogenic lineages in specific induction media. ASCs had the CD expression profile consistant with the International Federation for Adipose Therapeutics statement. The percentage of parent cells in PBMC after co-cultured with ASCs increased, though there was no statistical significance. However, when co-cultured with inflammatory priming ASCs, the percentage of parent cells significantly increased (with inflammatory priming ASCs group vs. without ASCs group, 38.7%±10.0% vs. 28.4%±8.9%, P<0.05). This indicated that inflammatory priming ASCs could significantly inhibit the proliferation of PBMCs. CONCLUSION: Inflammatory cytokines can enhance the immunosuppressive ability of ASCs. Our findings may help the application of ASCs in tissue repairment with better results.