Bassthomson7034

Prostate cancer (PCa) is the most common cancer type in men worldwide. Currently, the management of metastatic PCa (mPCa) remains a challenge to urologists. The analysis of hub genes and pathways may facilitate the understanding of the molecular mechanism of PCa. In the present study, to identify the hub genes in the mPCa, the three datasets GSE3325, GSE6919 and GSE38241 were downloaded from the platform of the Gene Expression Omnibus and function enrichment analysis of differentially expressed genes (DEGs) was performed. A total of 168 DEGs were obtained and the DEGs were significantly enriched in 'cell junction' and 'cell adhesion', among others. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis demonstrated that DEGs were enriched in three pathways including 'focal adhesion', 'renal cell carcinoma' and 'Hippo signaling pathway'. The results of the protein‑protein interaction network revealed that the hub genes in mPCa were separately PTEN, Rac GTPase‑activating protein 1, protein regulator of cytokinesis 1, PDZ binding kinase, centromere‑associated protein E, NUF2 component of NDC80 kinetochore complex, TPX2 microtubule nucleation factor, SOX2, CD44 and ubiquitin‑like with PHD and ring finger domains 1. As a hub gene, CD44 was differentially expressed in PCa, as determined by Oncomine analysis. Further experiments in vivo demonstrated that SB‑3CT, a selective matrix metalloproteinase inhibitor that has been reported to block CD44 cleavage and inhibit the downstream signaling pathway, suppressed the tumorigenicity of PCa cells by decreasing the expression levels of pyruvate dehydrogenase kinase 1 and 6‑phosphofructo‑2‑kinase/fructose‑2,6‑biphosphatase 4. Moreover, the combination therapy with SB‑3CT and docetaxel was more effective in inhibiting PCa compared with monotherapy. In conclusion, the identification of DEGs and the in vivo experimental results helped to elucidate the molecular mechanisms of PCa and provided a potential strategy for the treatment of PCa.Following the publication of this paper, the authors have requested that, on p. 4412 of the above article in the Funding section of the Declarations, the acknowledgement to one of the funding sources should be removed from the paper; essentially, the reference to grant no. 2018/31/B/NZ5/02475, formulated by the Polish National Science Centre (grant providing institution), should be removed from the paper. Therefore, the revised version of the Funding section paragraph should read as follows Funding The present study was supported by a grant from Poznan University of Medical Sciences (grant no. 502‑14‑02227367‑10694). The authors confirm that there are no further errors in the study, and all the authors agree to this correction. The authors are grateful to the Editor of Molecular Medicine Reports for granting them this opportunity to publish a Corrigendum, and apologize for any inconvenience caused. [the original article was published in Molecular Medicine Reports 20 4403-4414, 2019, DOI 10.3892/mmr.2019.10709].Ghrelin, an orexigenic hormone, is a peptide that binds to the growth hormone secretagogue receptor; it is secreted mainly by enteroendocrine cells in the oxyntic glands of the stomach. Ghrelin serves a role in both local and systemic physiological processes, and is implicated in various pathologies, including neoplasia, with tissue expression in several types of malignancies in both in vitro and in vivo studies. However, the precise implications of the ghrelin axis in metastasis, invasion and cancer progression regulation has yet to be established. In the case of gastrointestinal (GI) tract malignancies, ghrelin has shown potential to become a prognostic factor or even a therapeutic target, although data in the literature are inconsistent and unsystematic, with reports untailored to a specific histological subtype of cancer or a particular localization. Veliparib The evaluation of immunohistochemical expression shows a limited outlook owing to the low number of cases analyzed, and in vivo analyses have conflicting data regarding differences in ghrelin serum levels in patients with cancer. The aim of this review was to examine the relationship between ghrelin and GI tract malignancies to demonstrate the inconsistencies in current results and to highlight its clinical significance in the outcome of these patients.Accumulating evidence indicates that circular (circ)RNAs exhibit complex functions in diverse malignant tumors, including non‑small cell lung cancer (NSCLC). The role of the circRNA transcription adaptor 2A (circTADA2A) in NSCLC remains unclear. The expression, function and mechanism of circTADA2A in NSCLC development were investigated in the present study. The results revealed that circTADA2A was upregulated in NSCLC, and that knockdown of circTADA2A inhibited cell proliferation and migration in the NSCLC cell lines A549 and H1299. Functional assays demonstrated that circTADA2A promoted proliferation and migration via interacting with microRNA (miR)‑638. Bioinformatics and reverse transcription‑quantitative PCR assay confirmed that miR‑638 was expressed at low levels in NSCLC. In addition, it was found that miR‑638 served a tumor‑suppressive role and suppressed proliferation and migration via PCNA clamp associated factor (KIAA0101) inhibition in A549 and H1299 cells. Lastly, it was verified that circTADA2A promoted cell proliferation and migration, at least partially, via miR‑638/KIAA0101 signaling in A549 and H1299 cells. In summary, the present study showed that circTADA2A promoted NSCLC cell proliferation and migration via modulating miR‑638/KIAA0101 signaling.Spinal cord injury (SCI) is characterized by permanent motor deficits followed by inflammation and oxidative stress, causing neuronal cell death. The present study aimed to investigate the role of microRNA (miR)‑128 in neuronal cell apoptosis and its underlying mechanism. Targeting relationships among miR‑128 and Unc‑51 like autophagy activating kinase 1 (ULK1) and Fas ligand (FasL) were verified using dual‑luciferase reporter assay and ChIP assays. Loss‑ and gain‑of‑function assays were conducted in rat models of SCI to determine the roles of miR‑128 and ULK1 in neuronal cell apoptosis, inflammation, and motor function. Apoptosis, motor function and expression of inflammatory factors were respectively determined by Terminal deoxynucleotidyl transferase‑mediated dUTp nick end‑labeling, Basso, Beattie and Bresnahan (BBB) score and enzyme‑linked immunosorbent assay. Hematoxylin and eosin staining, Nissl staining and immunofluorescence were respectively performed to observe morphological changes and number of neurons and nestin‑positive cells.