Zinc finger protein 403 (ZFP403), located on human chromosome 17q12‑21, is closely associated with the development of cancer. However, to date, there are a limited number of studies on the biological functions of this gene, particularly in prostate cancer (PCa). The results of the present study demonstrated that compared with normal tissues, the expression of ZFP403 was markedly lower in PCa tissues, as shown by the evaluation of the Gene Expression Profiling Interactive Analysis 2 database. The decreased expression of ZFP403 in PCa clinical tissues and cell lines was confirmed by immunohistochemistry, reverse transcription‑quantitative PCR and western blot analysis. Using short harpin (sh)RNA inhibition, stably‑silenced ZFP403 cell lines were then constructed by lentiviral transfection (LV‑PC3‑shRNA‑1 and 2; LV‑DU145‑shRNA‑1 and 2). The results revealed that the knockdown of ZFP403 in PCa cells promoted cellular proliferation, colony formation, migration and invasiveness in vitro. Moreover, the levels of tumor growth‑ and motility‑related proteins were significantly altered after ZFP403‑knockdown. A xenograft tumor model using nude mice was established to elucidate the role of ZFP403 in tumorigenesis in vivo. Tumor growth was significantly increased in mice injected with ZFP403‑knockdown cells compared with the control mice. Overall, the findings of the present study demonstrate that ZFP403 functions as a tumor suppressor gene in PCa by affecting the proliferation, migration and invasiveness of PCa cells, suggesting its potential use as a clinical diagnostic marker.The transcription factor PU.1, an important member of the ETS family, plays a significant role in the differentiation of immune cells, which include macrophages, neutrophils, dendritic cells, T lymphoid cells, B lymphoid cells and so on. Immune cells are involved in the occurrence and development of diseases, including inflammatory diseases, neoplastic diseases and immune diseases. Therefore, it is particularly crucial to elucidate the roles and mechanisms of PU.1 in immune cells. The elucidation of these mechanisms may lead to the development of more effective therapeutic strategies for the treatment of inflammatory diseases and immune‑mediated diseases mediated by various immune cells. With the development of molecular biology, the mechanisms of PU.1 in immune cell differentiation have been further explained. Different levels of PU.1 expression determine the type of immune cell differentiation. PU.1 expression is increased during granulocyte and macrophage differentiation, while it is decreased during T lymphocyte and B lymphocyte differentiation. The present study reviews and discusses the effects of the transcription factor PU.1 on immune cell differentiation.Oleanolic acid (OA) is reported to possess antihypertensive activity via the regulation of lipid metabolism; however, the mechanisms underlying lipid regulation by OA are yet to be fully elucidated. The aim of the present study was to evaluate the mechanisms via which OA regulates lipid metabolism in spontaneously hypertensive rats (SHRs) via ultra‑performance liquid chromatography‑quadrupole/Orbitrap‑mass spectrometry (MS)‑based lipidomics analysis. SHRs were treated with OA (1.08 mg/kg) for 4 weeks. The liver tissues were excised, homogenized in dichloromethane and centrifuged, and subsequently the supernatant layer was collected and concentrated under vacuum to dryness. The dichloromethane extract was subjected to MS analysis and database searching, and comparison of standards was performed to identify potential biomarkers. Partial least squares‑discriminant analysis performed on the liver lipidome revealed a total of 14 endogenous metabolites that were significantly changed in the SHR model group (SH grout with OA resulted in significant improvements in blood pressure and associated abnormalities in the lipid metabolites.Aberrant methylation is one of the most frequent epigenetic alterations that regulate the expression levels of genes, including long non‑coding RNAs (lncRNAs), in tumors. However, to the best of our knowledge, the expression and function of hepatic nuclear factor 1α antisense RNA 1 (HNF1A‑AS1) and its methylation condition have not yet been reported in the development and progression of laryngeal squamous cell carcinoma (LSCC). In the present study, the expression and methylation of HNF1A‑AS1 were first examined by reverse transcription‑quantitative PCR, bisulfite genomic sequencing and methylation‑specific polymerase chain reaction in samples from patients with LSCC, which were based on the in silico analysis using The Cancer Genome Atlas data, and were then further verified in LSCC cell lines with and without 5‑Aza‑2'‑deoxycytidine (5‑Aza‑dC) treatment. Subsequently, proliferation, cell cycle distribution, migration and invasion of LSCC cells following either knockdown or overexpression of HNF1A‑AS1 were de cells. These findings suggested that HNF1A‑AS1 could serve as a tumor suppressor lncRNA in LSCC by regulating the EMT process, leading to the discovery of novel therapeutic targets and strategies for the treatment of patients with LSCC.Glycogen synthase kinase 3β (GSK 3β), a multifunctional serine and threonine kinase, plays a critical role in a variety of cellular activities, including signaling transduction, protein and glycogen metabolism, cell proliferation, cell differentiation, and apoptosis. Therefore, aberrant regulation of GSK 3β results in a broad range of human diseases, such as tumors, diabetes, inflammation and neurodegenerative diseases. Accumulating evidence has suggested that GSK 3β is correlated with tumorigenesis and progression. However, GSK 3β is controversial due to its bifacial roles of tumor suppression and activation. In addition, overexpression of GSK 3β is involved in tumor growth, whereas it contributes to the cell sensitivity to chemotherapy. However, the underlying regulatory mechanisms of GSK 3β in tumorigenesis remain obscure and require further in‑depth investigation. ATM/ATR inhibitor cancer In this review, we comprehensively summarize the roles of GSK 3β in tumorigenesis and oncotherapy, and focus on its potentials as an available target in oncotherapy.