BackgroundHuman bone marrow mesenchymal stem cells (hBMSCs) are implicated in cancer initiation and metastasis, sometimes by releasing exosomes that mediate cell communication by delivering microRNAs (miRNAs). This study aimed to investigate the physiological mechanisms by which exosomal miR-205 derived from hBMSCs may modulate the growth of prostate cancer cells.MethodsMicroarray-based gene expression profiling of prostate cancer was adopted to identify differentially expressed genes and regulatory miRNAs, which identified the candidates RHPN2 and miR-205 as the study focus. Then the binding affinity between miR-205 and RHPN2 was identified using in silico analysis and luciferase activity detection. Prostate cancer cells were co-cultured with exosomes derived from hBMSCs treated with either miR-205 mimic or miR-205 inhibitor. Subsequently, prostate cancer cell proliferation, invasion, migration, and apoptosis were detected in vitro. The effects of hBMSCs-miR-205 on tumor growth were investigated in vivo.ResultsmiR-205 was downregulated, while RHPN2 was upregulated in prostate cancer cells. RHPN2 was a target of miR-205, and upregulated miR-205 inhibited prostate cancer cell proliferation, invasion, and migration and promoted apoptosis by targeting RHPN2. Next, experiments demonstrated that hBMSCs-derived exosomes carrying miR-205 contributed to repressed prostate cancer cell proliferation, invasion, and migration and enhanced apoptosis. Furthermore, in vivo assays confirmed the inhibitory effects of hBMSCs-derived exosomal miR-205 on prostate cancer.ConclusionThe hBMSCs-derived exosomal miR-205 retards prostate cancer progression by inhibiting RHPN2, suggesting that miR-205 may present a predictor and potential therapeutic target for prostate cancer.

Prostate cancer (PCa) patients commonly present with osteoblastic‐type bone metastasis. Exosomes derived from tumor cells possess biological significance and can mediate intercellular communication in the tumor microenvironment. Long noncoding RNA (lncRNA) nuclear‐enriched abundant transcript 1 (NEAT1) is also implicated in the stability in tumorigenesis and the development of PCa, but the underlying mechanism remains elusive. Hence, the current study set out to investigate the physiological mechanisms by which exosomes‐encapsulated NEAT1 affects the progression of PCa. First, after isolation, we found PCa cell‐derived exosomes induced the osteogenic differentiation of human bone marrow‐derived mesenchymal stem cells (hBMSCs). Besides, NEAT1 in PCa cells could be transferred into hBMSCs via exosomes. Further gain‐ and loss‐of‐function experimentation revealed that NEAT1 acted as a competing endogenous RNA (ceRNA) of microRNA (miR)‐205‐5p to upregulate the runt‐related transcription factor 2 (RUNX2) levels. Moreover, NEAT1 could promote the RUNX2 expression via the splicing factor proline‐ and glutamine‐rich (SFPQ)/polypyrimidine tract‐binding protein 2 (PTBP2) axis. Functional assays uncovered that NEAT1 shuttled by PCa‐exosomes facilitated the activity of alkaline phosphatase (ALP) and mineralization of extracellular matrix, and continuously upregulated the levels of RUNX2, ALP, alpha‐1 type 1 collagen, and osteocalcin by regulating RUNX2, to induce the osteogenic differentiation of hBMSCs. Furthermore, in vivo experimentation confirmed that upregulated NEAT1 induced osteogenesis. Collectively, our findings indicated that PCa‐derived exosomes‐loaded NEAT1 upregulated RUNX2 to facilitate the osteogenesis of hBMSCs by competitively binding to miR‐205‐5p via the SFPQ/PTBP2 axis, therefore providing a potential therapeutic target to treat osteogenesis of hBMSCs in PCa. PCa cells secrete exosomes containing NEAT1, and NEAT1 exerts effects on osteogenic differentiation of hBMSCs in PCa. NEAT1 shuttled by PCa‐derived exosomes could be transferred into hBMSCs, where NEAT1 exerted inductive properties in osteogenic differentiation of hBMSCs through the upregulation of RUNX2 by competitively binding to miR‐205‐5p and regulating SFPQ/PTBP2 in vitro and in vivo .

Aims: Juxtaglomerular cell tumor is a rare kidney tumor. This study aimed to report the clinic features of juxtaglomerular cell tumor and our treatment experience. Methods: The medical records of 9 juxtaglomerular cell tumor patients treated in our hospital from 1997 to 2017 were retrospectively reviewed. Clinical characteristics, immunohistochemical findings, treatments and outcomes were collected. Results: The mean age of 9 patients was 24±8.1 years (range: 18-37). All cases had symptoms of hypertension, hyperaldosteronism, high plasma renin, high plasma angiotensin II. Four cases had hypokalemia. The renal masses were found by enhanced contrast tomography in all patients. One case received ultrasound-guided ablation and was clinically diagnosed with juxtaglomerular cell tumor. Among the remaining 8 cases, 2 cases received nephrectomy while 6 underwent partial nephrectomy. The 8 cases were pathologically diagnosed with juxtaglomerular cell tumor. Immunohistochemical findings showed that juxtaglomerular cell tumor was positive for vimentin, CD34, and actin but negative for chromogranin A. After treatment, all the patients had normal levels of blood pressure, serum renin activity, potassium, and aldosterone. No patients had tumor progress or metastasis within a median follow-up period of 94 (range: 33-241) months. Conclusion: Hypertension combined with hyperaldosteronism and hypokalemia secondary to high plasma renin activity are the typical symptoms of juxtaglomerular cell tumor. Partial nephrectomy is an optimal treatment for juxtaglomerular cell tumor.

The aim of the present study was to predict key genes and proteins associated with complex regional pain syndrome (CRPS) using bioinformatics analysis. The gene expression profiling microarray data, GSE47603, which included peripheral blood samples from 4 patients with CRPS and 5 healthy controls, was obtained from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) in CRPS patients compared with healthy controls were identified using the GEO2R online tool. Functional enrichment analysis was then performed using The Database for Annotation Visualization and Integrated Discovery online tool. Protein‑protein interaction (PPI) network analysis was subsequently performed using Search Tool for the Retrieval of Interaction Genes database and analyzed with Cytoscape software. A total of 257 DEGs were identified, including 243 upregulated genes and 14 downregulated ones. Genes in the human leukocyte antigen (HLA) family were most significantly differentially expressed. Enrichment analysis demonstrated that signaling pathways, including immune response, cell motion, adhesion and angiogenesis were associated with CRPS. PPI network analysis revealed that key genes, including early region 1A binding protein p300 (EP300), CREB‑binding protein (CREBBP), signal transducer and activator of transcription (STAT)3, STAT5A and integrin α M were associated with CRPS. The results suggest that the immune response may therefore serve an important role in CRPS development. In addition, genes in the HLA family, such as HLA‑DQB1 and HLA‑DRB1, may present potential biomarkers for the diagnosis of CRPS. Furthermore, EP300, its paralog CREBBP, and the STAT family genes, STAT3 and STAT5 may be important in the development of CRPS.

PurposeSurgical removal of pheochromocytoma (PCC), including open, laparoscopic, and robot-assisted adrenalectomy, is the cornerstone of therapy, which is associated with high risk of intraoperative and postoperative life-threatening complications due to intraoperative hemodynamic instability (IHD). This study aims to develop and validate a nomogram based on clinical characteristics as well as computed tomography (CT) features for the prediction of IHD in pheochromocytoma surgery.MethodsThe data from 112 patients with pheochromocytoma were collected at a single center between January 1, 2010, and December 31, 2019. Clinical and radiological features were selected with the least absolute shrinkage and selection operator regression analysis to predict IHD then constitute a nomogram. The performance of the nomogram was assessed in terms of discrimination, calibration, and clinical utility.ResultsAge, tumor shape, Mayo Adhesive Probability score, laterality, necrosis, body mass index, and surgical technique were identified as risk predictors of the presence of IHD. The nomogram was then developed using these seven variables. The model showed good discrimination with a C-index of 0.773 (95% CI, 0.683–0.862) and an area under the receiver operating characteristic curve (AUC) of 0.739 (95% CI, 0.642–0.837). The calibration plot suggested good agreement between predicted and actual probabilities. Besides, calibration was tested with the Hosmer–Lemeshow test (P = 0.961). The decision curve showed the clinical effectiveness of the nomogram.ConclusionsOur nomogram based on clinical and CT parameters could facilitate the treatment strategy according to assessment of the risk of IHD in patients with pheochromocytoma.