Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer.

Prostate cancer (PCa) is one of the most common malignancies among males worldwide. Anti-silencing function 1B histone chaperone (ASF1B) has been reported to be involved in PCa. The present study aimed to investigate the role and molecular mechanism of ASF1B in PCa. Data of genes were obtained from The Cancer Genome Atlas database. The core gene was identified using the DAVID website. Cell viability and colony formation were detected using a cell counting kit-8 assay and crystal violet staining, respectively. Cell cycle distribution and apoptosis were assessed using flow cytometry analysis. The corresponding factors were analyzed by reverse transcription-quantitative polymerase chain reaction and western blotting. It was demonstrated that ASF1B was highly expressed in the PCa tissues and cells compared with the non-PCa tissues and cells, respectively. While siRNA-ASF1B significantly reduced the viability and colony formation, it promoted apoptosis, G1 phase cell cycle arrest of LNCap as well as C4-2 cells. siRNA-ASF1B was revealed to significantly reduce the level of B-cell lymphoma-2 and cyclin D1, and enhance the expression levels of p53, caspase-3 and Bcl-2 associated X protein. Furthermore, the phosphorylation levels of phosphatidylinositol 3 kinase (PI3K) and protein kinase B (Akt) were significantly decreased in the siRNA-ASF1B group compared with the mock group. In summary, the present study demonstrated that silencing of ASF1B suppressed the proliferation, and promoted apoptosis and cell cycle arrest of PCa cells. Inhibition of the PI3K/Akt signaling pathway was pertinent to the role of si-ASF1B. This phenomenon suggests that the downregulation of ASF1B may aid in inhibiting the progression of PCa.

Silencing of URG11 expression inhibits the proliferation and epithelial­mesenchymal transition in benign prostatic hyperplasia cells via the RhoA/ROCK1 pathway.

Upregulated gene 11 (URG11) represents a gene upregulated by hepatitis B virus X protein and is involved in the biological processes of multifarious tumors. The present study aimed to investigate the protective effects and regulatory mechanisms of URG11 in benign prostatic hyperplasia (BPH). URG11, Ras homolog family member A (RhoA) and Rho­associated protein kinase 1 (ROCK1) expression was detected in patients with BPH using reverse transcription­quantitative polymerase chain reaction (RT­qPCR). Furthermore, URG11 expression was silenced using URG11­targeting small interfering RNAs. In addition, cell viability was determined by performing a Cell Counting Kit­8 assay, and the effect of URG11 on the cell cycle was investigated by flow cytometry. Expression levels of cyclin D1, p27, E­cadherin, N­cadherin, vimentin, RhoA and ROCK1 were investigated by RT­qPCR and western blotting. The results revealed that the expression levels of URG11, RhoA and ROCK1 were enhanced in patients with BPH­1 cells compared with matched healthy controls. Furthermore, it was demonstrated that transforming growth factor­ß (TGF­ß) induced the proliferation of BPH­1 cells in vitro, and silencing of URG11 inhibited the effects of TGF­ß on BPH­1 cell proliferation and the cell cycle. In addition, silencing of URG11 altered the expression levels of cell cycle­associated genes, epithelial­mesenchymal transition­associated genes, and RhoA and ROCK1 protein levels. Thus, the results of the present study suggest that URG11 may be a potential therapeutic target, which may be important to inhibit the development and progression of prostatic hyperplasia.

Long non-coding RNA FENDRR reduces prostate cancer malignancy by competitively binding miR-18a-5p with RUNX1.

CONTEXT: Prostate cancer (PCa) is one of the most commonly diagnosed malignancy in men in the western world. OBJECTIVE: We aim to investigate the biological role of long non-coding RNA FENDRR and its mechanism in PCa. MATERIALS AND METHODS: We determined the expression of FENDRR and miR-18a-5p in PCa tissues and examined the regulatory mechanism in PCa cell lines. RESULTS: FENDRR transcripts in human PCa tissues were significantly decreased compared with the normal controls. Reduced expression of FENDRR was correlated with the increase of pathological degree and poor prognosis in PCa patients. Upregulation of FENDRR inhibited cell proliferation, increased apoptosis and decreased invasion and migration ability, which was inhibited by miR-18a-5p mimic. Knockdown of FENDRR resulted in a significant increase of PCa cell proliferation and decrease of apoptosis and this effect was inhibited miR-18a-5p inhibitor. FENDRR and RUNX1 contain potential target sites for miR-18a-5p. miR-18a-5p mimic inhibited RUNX1 expression and luciferase activity. FENDRR could increase RUNX1 expression, which was inhibited by miR-18a-5p. The effect of FENDRR on cell proliferation, apoptosis and invasion and migration ability was suppressed by silence of RUNX1. DISCUSSION AND CONCLUSION: These results position FENDRR/miR-18a-5p/RUNX1 as a potential therapeutic target and biomarker for PCa.

Renal pelvis urothelial carcinoma of the upper moiety in complete right renal duplex: a case report.

Urothelial carcinoma (UC) originated from renal pelvis is the common tumor of the urinary system, however, neoplasia of the renal pelvis in duplex kidneys is extremely rare, especially in the complete renal and ureteral duplex cases. We present the first case of renal pelvis UC of the upper moiety in a complete right renal duplex. This male patient has bilateral complete renal and ureteral duplex. To the best of our knowledge, this is the first reported case of renal pelvis UC in a complete renal duplex system. After this experience we feel that the diagnosis of renal pelvis UC in duplex kidneys is not so easy, and once the diagnosis is determined, the whole renal duplex units and bladder cuff or ectopic orifice should be excised radically.