Circular RNAs (circRNAs) are a class of non‑coding RNAs formed by covalently closed loops through back‑splicing and exon‑skipping. circRNAs have been confirmed to play a vital role in various biological functions, acting as microRNA sponges and reservoirs, as well as combining with RNA‑binding proteins during the progression of multiple cancer types. Therefore, the present review evaluated recent research articles in PubMed that were published between November 2017 and September 2020. Key word search strings included 'Circular RNA (circRNA) AND bladder cancer (BC)', 'circular RNA (circRNA) AND prostate cancer (PCa)' and 'circular RNA (circRNA) AND renal cell cancer (RCC)'. In total, >58 circRNAs were found to be implicated in urological cancers, with several of the circRNAs targeting common carcinogenic pathways, such as the AKT, TGF‑β, MAPK, VEGF and even metabolic pathways. https://www.selleckchem.com/products/OSI-906.html circRNAs are important modulators of BC, PCa and RCC. circRNAs are functionally implicated in the pathogenesis of these cancer types, and have been found to act as biomarkers for the diagnosis and prognosis of urological cancer. However, to the best of our knowledge, the functions of circRNAs in tumors of the urinary system remain largely unknown and require further research.Pituitary tumors do not pose a threat to life but can cause visual disturbances and serious clinical syndromes, such as infertility and metabolic syndrome. Therefore, screening of key genes involved in the occurrence and development of pituitary tumors can provide new targets for the treatment of pituitary tumors. The aim of the present study was to investigate the molecular mechanism of long non‑coding (lnc.) RNA maternally expressed 3 (MEG3) in cell proliferation, apoptosis and epithelial‑mesenchymal transition (EMT) processes of pituitary tumor. Tissue samples were obtained from 34 patients who underwent surgical treatment of pituitary tumors. Pituitary tumor cells (GH3 and MMQ) were transfected with pcDNA3.1(+)‑MEG3, short hairpin (sh)MEG3, microRNA (miR)‑23‑3p inhibitor or their controls using Lipofectamine® 2000. Reverse transcription‑quantitative PCR and western blot analyses were used to detect the levels of MEG3, miR‑23b‑3p and FOXO4, as well as proliferation‑, apoptosis‑ and EMT‑associated genes andmor development by participating in cell proliferation, apoptosis and the EMT process, which may present a novel target for pituitary tumor treatment.Glioblastoma is the most common and aggressive brain tumor and it is characterized by a high mortality rate. Temozolomide (TMZ) is an effective chemotherapy drug for glioblastoma, but the resistance to TMZ has come to represent a major clinical problem, and its underlying mechanism has yet to be elucidated. In the present study, the role of exosomal connexin 43 (Cx43) in the resistance of glioma cells to TMZ and cell migration was investigated. First, higher expression levels of Cx43 were detected in TMZ‑resistant U251 (U251r) cells compared with those in TMZ‑sensitive (U251s) cells. Exosomes from U251s or U251r cells (sExo and rExo, respectively) were isolated. It was found that the expression of Cx43 in rExo was notably higher compared with that in sExo, whereas treatment with rExo increased the expression of Cx43 in U251s cells. Additionally, exosomes stained with dioctadecyloxacarbocyanine (Dio) were used to visualized exosome uptake by glioma cells. It was observed that the uptake of Dio‑stained rExo in U251s cells was more prominent compared with that of Dio‑stained sExo, while 37,43Gap27, a gap junction mimetic peptide directed against Cx43, alleviated the rExo uptake by cells. Moreover, rExo increased the IC50 of U251s to TMZ, colony formation and Bcl‑2 expression, but decreased Bax and cleaved caspase‑3 expression in U251s cells. 37,43Gap27 efficiently inhibited these effects of rExo on U251s cells. Finally, the results of the wound healing and Transwell assays revealed that rExo significantly enhanced the migration of U251s cells, whereas 37,43Gap27 significantly attenuated rExo‑induced cell migration. Taken together, these results indicate the crucial role of exosomal Cx43 in chemotherapy resistance and migration of glioma cells, and suggest that Cx43 may hold promise as a therapeutic target for glioblastoma in the future.Environmental endocrine disruptor chemicals are substances that can alter the homeostasis of the endocrine system in living organisms. They can be released from several products used in daily activities. Once in the organism, they can disrupt the endocrine function by mimicking or blocking naturally occurring hormones due to their similar chemical structure. This endocrine disruption is the most important cause of the well‑known hormone‑associate types of cancer. Additionally, it is decisive to determine the susceptibility of each organ to these compounds. Therefore, the present review aimed to summarize the effect of different environmental substances such as bisphenol A, dichlorodiphenyltrichloroethane and polychlorinated biphenyls in both the mammary and the prostate tissues. These organs were chosen due to their association with the hormonal system and their common features in carcinogenic mechanisms. Outcomes derived from the present review may provide evidence that should be considered in future debates regarding the effects of endocrine disruptors on carcinogenesis.Sirtuin 1 (SIRT1), a member of the sirtuin protein family, is a nicotinamide adenine dinucleotide (NAD+)‑dependent type III histone deacetylase and mono‑ADP‑ribosyltransferase. SIRT1 can deacetylate histones (H1, H3, and H4) and non‑histone proteins, and it is widely involved in various physiological and pathological processes in the body, including metabolism, aging, transcription, DNA damage and repair, apoptosis, cell cycle regulation, inflammation and cancer. Research has shown that SIRT1 is involved in tumorigenesis, tumor metastasis and chemotherapy resistance, but it exerts opposing effects and plays different roles in different pathogenic processes. Recent studies have demonstrated that SIRT1 may be implicated in the pathogenesis, development, treatment and prognosis of tumors; however, its role in gynecological tumors remains elusive. The aim of the present review was to summarize the pathogenic roles of SIRT1 in cancer, and to provide what is, to the best of our knowledge, the first review of recent advances involving SIRT1 in cervical cancer, endometrial cancer (EC) and ovarian cancer (OC).