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Common chromophobe renal cell carcinoma (chRCC) has a good prognosis when cured by surgery. However, clinical practice shows that a small number of patients with chRCC will produce metastasis, and the prognosis after metastasis is poor. In this regard, we try to find potential biological targets to prevent CRCC metastasis. In this experiment, we analyzed the clinical traits and gene expression data of chRCC samples which were provided by the TCGA database by the WGCNA method. On this basis, we selected MEtan, a module with a significant positive correlation with the M phase of chRCC, for subsequent analysis. The MEtan module genes in the biological process of chRCC were mainly related to steroid metabolic process, cholesterol metabolic process and STEM cell differentiation. KEGG analysis showed that these genes were mainly enriched in cancer-related signaling pathways, such as Neuroactive Ligand−receptor interaction, cAMP signaling pathway, and Wnt signaling pathway. Subsequently, we mapped the PPI interaction network and screened the key gene beta-arrestin 2 (ARRB2). Expression analysis showed that there was a significantly increased expression of ARRB2 in chRCC patients in comparison to the normal group. Expression survival analysis indicated that ARRB2 was inversely associated with overall survival. We firmly believe that the key genes identified in this study would be able to provide new clues and research basis for the treatment of chRCC. [ABSTRACT FROM AUTHOR]

Objective. To evaluate the effects of human bone marrow mesenchymal stem cells (hBMSCs) and osteoblasts (hFOB1.19) on PC3 prostate cancer cells. Methods. To simulate the in vivo interaction between the bone/bone marrow microenvironments and prostate cancer cells, we established cocultures of PC3 cells with hBMSC or hFOB1.19 cells and evaluated their effects on the proliferation, cell cycle distribution, cell migration, and invasion of PC3 cells. Quantitative reverse transcription polymerase chain reaction was used to detect CD59 mRNA expression in PC3 cells. The expression of receptor activator of nuclear factor- (NF-) κB (RANK), RANK ligand (RANKL), osteoprotegerin (OPG), CD59, NF-κB (p50 subunit), and cyclin D1 in PC3 cells was analyzed by immunofluorescence and western blotting. Results. hBMSCs and hFOB1.19 cells enhanced the proliferation, migration, and invasion of PC3 cells; increased the proportion of PC3 cells in the S and G2/M phases of the cell cycle; and upregulated RANK, RANKL, OPG, CD59, cyclin D1, and NF-κB (p50 subunit) expression by PC3 cells. The RANKL inhibitor, scutellarin, inhibited these effects in PC3-hFOB1.19 cocultures. Conclusion. hBMSCs and hFOB1.19 cells modulate the phenotype of PC3 prostate cancer cells and the expression of CD59 by activating the RANK/RANKL/OPG signaling pathway. [ABSTRACT FROM AUTHOR]