The clinical significance and underlying molecular mechanism of miRNA-222-3p in metastatic prostate cancer (MPCa) remain unclear. The present study used a large number of cases (n = 1,502) based on miRNA chip and miRNA sequencing datasets to evaluate the expression and diagnostic potential of miRNA-222-3p in MPCa. We applied a variety of meta-analytic methods, including forest maps, sensitivity analysis, subgroup analysis and summary receiver operating characteristic curves, to prove the final results. MiRNA-222-3p was reduced in MPCa and had a moderate diagnostic potential in MPCa. We screened 118 miRNA-222-3p targets using three different methods including miRNA-222-3p transfected MPCa cell lines, online prediction databases and differently upregulated genes in MPCa. Moreover, functional enrichment analysis performed to explore the potential molecular mechanism of miRNA-222-3p showed that the potential target genes of miRNA-222-3p were significantly enriched in the p53 signal pathway. In the protein-protein interaction network analysis, SNAP91 was identified as a hub gene that may be closely related to MPCa. Gene chip and RNA sequencing datasets containing 1,237 samples were used to determine the expression level and diagnostic potential of SNAP91 in MPCa. SNAP91 was found to be overexpressed in MPCa and had a moderate diagnostic potential in MPCa. In addition, miRNA-222-3p expression was negatively correlated with SNAP91 expression in MPCa (r = −0.636, P = 0.006). These results demonstrated that miRNA-222-3p might play an important role in MPCa by negatively regulating SNAP91 expression. Thus, miRNA-222-3p might be a potential biomarker and therapeutic target of MPCa.

Background SCL/TAL1 interrupting locus (STIL) is associated with the progression of several tumors; however, the biological role of STIL in osteosarcoma remains poorly understood. Methods In this study, the clinical significance of STIL in osteosarcoma was analyzed by gene chip data recorded in public databases. STIL expression was silenced in osteosarcoma cell lines to observe the effects on proliferation, apoptosis, invasion, and migration. Differentially expressed genes (DEGs) in the osteosarcoma chip were analyzed using The Limma package, and STIL co-expressed genes were obtained via the Pearson correlation coefficient. The potential molecular mechanism of STIL in osteosarcoma was further explored by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Results Osteosarcoma was associated with higher STIL expression compared to the control samples, and the standardized mean difference (SMD) was 1.52. STIL also had a good ability to distinguish osteosarcoma from non-osteosarcoma samples [area under the curve (AUC) = 0.96]. After silencing STIL, osteosarcoma cell proliferation decreased, apoptosis increased, and the migratory and invasion ability decreased. A total of 294 STIL differentially co-expressed genes were screened, and a bioinformatics analysis found that differentially co-expressed genes were primarily enriched in the cell signaling pathways. The protein-protein interaction (PPI) network indicated that the hub differentially co-expressed genes of STIL were CDK1, CCNB2, CDC20, CCNA2, BUB1, and AURKB. Conclusions STIL is associated with osteosarcoma proliferation and invasion, and may be promote the progression of osteosarcoma by regulating the expression of CDK1, CCNB2, CDC20, CCNA2, BUB1 and AURKB.

Background: KIAA1429, a member of the RNA methyltransferase complex, is involved in cancer progression. However, the clinical significance of KIAA1429 in osteosarcoma (OS) and the underlying mechanisms by which it contributes to disease progression remain unclear. Methods: The clinical significance of KIAA1429 in OS was evaluated based on the RT-qPCR, microarray, RNA sequencing, and published data. Two lentivirus-mediated KIAA1429-targeting siRNA constructs were transfected into SW1353 cells, and CCK-8 and flow cytometry assays were applied to investigate the biological function of KIAA1429 in OS cells. KIAA1429-related genes in OS were identified from lists of co-expressed genes (CEGs) and differentially expressed genes (DEGs). Functional enrichment analysis was employed to explore the potential mechanisms by which KIAA1429 contributes to the progression of OS.Results: The mRNA expression of KIAA1429 was notably overexpressed in 250 OS samples than 71 non-cancer samples (SMD=0.74). SROC curve analysis showed that KIAA1429 exhibits diagnostic capacity between OS samples and non-cancer samples (AUC=0.83). Survival analysis showed that overexpression of KIAA1429 was associated with shorter overall survival time. Knocking down KIAA1429 reduced the level of m6A methylation, inhibited proliferation, and accelerated apoptosis in OS cells. A total of 395 KIAA1429-related genes were identified, and were enriched in the cell cycle pathway. Protein–protein interaction (PPI) network analysis showed that CDK1, CCNA2, and CCNB1 were KIAA1429-related genes that act as major network hubs in OS. Conclusion: KIAA1429 plays an oncogenic role in OS and may facilitate the progression of OS through a mechanism involving the regulation of CDK1, CCNA2, and CCNB1.