Endocrine therapy for prostate cancer (PCa) mainly inhibits androgen receptor (AR) signaling, due to increased androgen synthesis and AR changes, PCa evolved into castration-resistant prostate cancer (CRPC). The function of Family With Sequence Similarity 64 Member A (FAM64A) and its association with prostate cancer has not been reported. In our research, we first reported that FAM64A is up-regulated and positively associated with poor prognosis of patients with prostate cancer (PCa) by TCGA database and immunohistochemistry staining. Moreover, knockdown of FAM64A significantly suppressed the proliferation, migration, invasion, and cell cycle of PCa cells in vitro. Mechanistically, FAM64A expression was increased by dihydrotestosterone (DHT) through direct binding of AR to FAM64A promoter, and notably promoted the proliferation, migration, invasion, and cell cycle of androgen-dependent cell line of PCa. In addition, abnormal expression of FAM64A affects the immune and interferon signaling pathway of PCa cells. In conclusion, FAM64A was up-regulated by AR through directly binding to its specific promoter region to promote the development of PCa, and was associated with the immune mechanism and interferon signaling pathway, which provided a better understanding and a new potential for treating PCa.

Aptazyme and CRISPR/Cas gene editing system were widely used for regulating gene expression in various diseases, including cancer. This work aimed to reconstruct CRISPR/Cas13d tool for sensing hTERT exclusively based on the new device OFF-switch hTERT aptazyme that was inserted into the 3’ UTR of the Cas13d. In bladder cancer cells, hTERT ligand bound to aptamer in OFF-switch hTERT aptazyme to inhibit the degradation of Cas13d. Results showed that engineered CRISPR/Cas13d sensing hTERT suppressed cell proliferation, migration, invasion and induced cell apoptosis in bladder cancer 5637 and T24 cells without affecting normal HFF cells. In short, we constructed engineered CRISPR/Cas13d sensing hTERT selectively inhibited the progression of bladder cancer cells significantly. It may serve as a promising specifically effective therapy for bladder cancer cells.

MiRNAs have been reported to be involved in multiple cellular processes and the tumorigenesis of various cancers. miR‑15a‑5p (also termed miR‑15a) has previously been determined to be upregulated in renal cell carcinoma (RCC) by microarray profile. However, the expression and function of miR‑15a‑5p in RCC remain to be validated. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to detect the expression levels of miR‑15a‑5p in RCC tissues and cells. The expression level of miR‑15a‑5p was upregulated or downregulated by transfecting synthesized miR‑15a‑5p mimics or inhibitors. The MTT assay, CCK‑8 assay, Transwell assay, wound healing assay, Hoechest 33342 staining and flow cytometry were conducted to investigate the role of miR‑15a‑5p in RCC. The results of the RT‑qPCR demonstrated that miR‑15a‑5p was upregulated in RCC tissues and ACHN, 786‑O and 769P RCC cells compared with paired normal tissues and HEK‑293T cells. miR‑15a‑5p was observed to be associated with RCC cell proliferation, migration, invasion and apoptosis. The results demonstrated that miR‑15a‑5p may be important as a tumor promoter in RCC. To the best of our knowledge, the present study is the first to describe miR‑15a‑5p as a tumor promoter in RCC. Further research will be performed to investigate the underlying signaling pathway of miR‑15a‑5p and the potential role of miR‑15a‑5p as a biomarker for early detection, prognosis prediction and a therapeutic target of RCC.

A rare neoplasm, termed ‘anastomosing hemangioma’ (AH), has been previously described in the genitourinary tract. To date, 29 cases of AH have been reported in the literature, and the case reported in the present study is, to the best of our knowledge, the first AH described in the urinary bladder. It is essential to distinguish AH from malignant vascular tumors due to the different treatments required and the prognosis. The patient in this case study was asymptomatic, with a neoplasm of ~1 cm within the right wall of the bladder. Pathologically, the lesion was predominantly composed of a structure comprising a small vascular cavity and irregularly fenestrated anastomosing vascular channels, with no clear atypia of the endothelial cells.

MicroRNAs (miRs) are small, endogenous noncoding RNAs that serve a significant function in various biologic processes, including those involved in cancer. The present study aimed to determine the expression and function of miR-16 in renal cell carcinoma (RCC). Quantitative polymerase chain reaction was used to quantify the expression of miR-16 in 48 paired RCC tissues and adjacent normal tissues. The impact of miR-16 on cell proliferation, migration and apoptosis was analyzed by transfecting miR-16 mature molecules into the renal cancer cell lines 786-O and ACHN. The results indicated that miR-16 was significantly upregulated in RCC tissues (P<0.05). Downregulation of miR-16 resulted in reduced cell proliferation and migration and increased levels of apoptosis, while overexpression of miR-16 resulted in accelerated cellular proliferation and migration, suggesting that miR-16 may function as an oncogene in RCC. The present study demonstrated for the first time, to the best of our knowledge, that miR-16 is upregulated in RCC and acts as an oncogene by inducing cellular proliferation, migration and reducing apoptosis. Further study of miR-16 in RCC may clarify the molecular mechanisms of RCC carcinogenesis and aid in the development of novel biomarkers and therapeutic options.