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.

Silencing of URG11 expression inhibits the proliferation and epithelial‑mesenchymal 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 Rho‑associated protein kinase 1 (ROCK1) expression was detected in patients with BPH using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR).

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.

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.