BackgroundProstate cancer (PCa) is one of the most malignant tumors of the male urogenital system. There is an urgent need to identify novel biomarkers for PCa.MethodsIn this study, we evaluated the expression levels of MCM10 in prostate cancer by analyzing public datasets (including The Cancer Genome Atlas and GSE21032). Furthermore, loss of function assays was performed to evaluate the effects of MCM10 on cell proliferation, apoptosis, and colony formation. Furthermore, we performed microarray and bioinformatics analyses to explore the potential mechanisms of MCM10.ResultsIn the present study, we for the first time revealed MCM10 was significantly upregulated in PCa. Moreover, we found increased MCM10 expression was significantly associated with advanced clinical stage and high Gleason score PCa. Kaplan‐Meier analysis demonstrated higher MCM10 expression was associated with a poorer patient prognosis in PCa. Furthermore, loss of function assays showed that MCM10 knockdown inhibited cell proliferation and colony formation, but promoted cell apoptosis. Additionally, we performed microarray and bioinformatics analysis and found MCM10 regulated PCa progression by regulating a series of biological processes including cancer, cell death, and apoptosis.ConclusionsThese results suggest that MCM10 may be a potential diagnostic and therapeutic target for PCa.

Prostate cancer (PCa) is one of the most frequently diagnosed types of cancer worldwide. However, there remains a lack of accurate biomarkers to predict the outcome of PCa. Non-SMC condensin I complex subunit H (NCAPH) encodes a regulatory subunit of the non-structural maintenance of chromosomes condensin I complex. The present study aimed to investigate whether NCAPH may be a novel diagnostic marker for PCa by analyzing public datasets, including GSE17951, GSE55945 and a dataset from The Cancer Genome Atlas. The current results, to the best of our knowledge, demonstrated for the first time that NCAPH is significantly upregulated in PCa. Furthermore, it was identified that NCAPH expression is higher in stage T3/T4 and N1 PCa samples compared with stage T2 and N0 PCa samples, respectively. Kaplan-Meier analysis demonstrated that overexpression of NCAPH is associated with poor survival of patients with PCa. Bioinformatics analysis revealed that NCAPH is involved in regulating the PCa cell cycle by interacting with a number of proteins, including non-SMC condensin I complex subunit D2, non-SMC condensin I complex subunit G, structural maintenance of chromosomes 4, structural maintenance of chromosomes 2, Aurora kinase A, Aurora kinase B, cyclin-dependent kinase 1, H2A histone family member Z, POC1 centriolar protein A and histone cluster 2 H2A family member C. In summary, the present results suggest NCAPH may be a novel and beneficial diagnostic and therapeutic target in PCa.

Prostate cancer (PCa) is the most frequently diagnosed type of cancer in Chinese males. Cell-cycle aberration is a hallmark of cancer. Spindle pole body component 25 homolog (SPC25), a component of the Ndc80 complex, serves an important role in regulating mitotic chromosome segregation. However, the functional roles of SPC25 in PCa remain poorly understood. To the best of our knowledge, the present study was the first to demonstrate that SPC25 is significantly upregulated in PCa. In order to investigate the molecular roles of SPC25, a loss of function assay was performed, revealing that SPC25 knockdown inhibited cell proliferation, and induced a decrease in the number of cells in the S phase and an increase in the number of cells in the G2/M phase. Furthermore, SPC25 knockdown promoted the apoptosis of PCa cells. Additionally, bioinformatics analysis revealed multiple functional roles of SPC25 in regulating cell proliferation, apoptosis, invasion, transforming growth factor-β signaling and the SUMOylation pathway in PCa. The present study also evaluated the potential prognostic value of SPC25 using The Cancer Genome Atlas RNA-seq data and demonstrated that SPC25 was upregulated in late stage PCa. Kaplan-Meier analysis demonstrated that lower SPC25 expression was associated with an improved survival rate in patients with PCa. Taken together, these results suggested that SPC25 serves an oncogenic role in PCa and may act as a novel diagnostic and therapeutic target for PCa.

Hierarchical MnCo2S4/FeCo2S4 “lollipops” constructed by nanosheet-built MnCo2S4 microspheres and FeCo2S4 nanoneedles were synthesized and immobilized on hollow carbon skeleton for efficient energy storage.

Globally, prostate cancer is the most common malignancy among men and there is no biomarker for defining tumour invasion and progression. Guanosine-5'-triphosphate (GTP)-binding RAS-like 3 (ARHI) is a tumour suppressor gene that has been found to be downregulated in the prostate cancer cell line PC-3. MicroRNA 221 and 222 have been shown to regulate ARHI expression negatively. This study evaluated tissue samples from patients with prostate cancer (n = 35) that were designated as aggressive or non-aggressive according to their Gleason grade. Expression of ARHI and microRNA 221 and 222 was measured by real-time reverse transcription-polymerase chain reaction. The level of ARHI mRNA was significantly lower in aggressive compared with non-aggressive prostate cancer tissue samples. In contrast, microRNA 221 and 222 levels were significantly higher in aggressive compared with non-aggressive prostate cancer tissue samples. Whether ARHI and microRNA 221 and 222 could be considered as biomarkers for disease progression in prostate cancer requires further investigation.