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TSTA3 upregulation significantly enhanced β‑catenin expression and promoted its nuclear accumulation. In addition, TSTA3 expression was negatively regulated by miR‑125a‑5p, which was downregulated in lung cancer. Furthermore, TSTA3 overexpression markedly promoted cell proliferation, migration, invasion and tumorigenesis, and suppressed cell apoptosis. AZ 3146 cost TSTA3 downregulation abolished the effects of miR‑125a‑5p downregulation on promoting lung cancer cell malignant transformation. Overall, the current study demonstrates that TSTA3 is regulated by miR‑125a‑5p and functions as an oncogene in lung cancer via promoting the activation of β‑catenin signaling.Although the COVID‑19 epidemic has lasted for months, it has not yet been successfully controlled, and little is known about neonatal COVID‑19. Therefore, literature search was conducted for references in PubMed, Science Direct, ProQuest, Web of Science and China National Knowledge Infrastructure for detailed case reports on neonatal COVID‑19 published as of July 15, 2020, to facilitate the clinical treatment, epidemic prevention and control of neonatal COVID‑19. Forty nonoverlapping case reports focusing mainly on the demographic characteristics, transmission modes, clinical features, treatments and prognosis of neonatal COVID‑19, including 3 in Chinese and 37 in English, were available.Sepsis‑induced cardiorenal syndrome is one of the multiple organ dysfunctions observed in sepsis. It is determined by a primary dysfunction in one organ that leads to secondary injury to another organ. Studies have shown the involvement of microRNAs (miRs) in the diagnosis and prognosis of several pathologies. However, the implication of miR‑126 in the podocyte damage associated with sepsis has not been evaluated until now. In the current study, the miR‑126 expression was downregulated in a podocyte injury model together with downregulation of nephrin expression. The transfection of podocytes from podocyte injury group with miR‑126 mimics demonstrated an increase in cell proliferation and a decrease in cell apoptosis. Bioinformatics analysis predicted that the target of miR‑126 was epidermal growth factor‑like domain multiple 6 (EGFL6) and dyskeratosis congenita 1 (DKC1) and these were confirmed by dual‑luciferase reporter assay. miR‑126 upregulation determined EGFL6 and DKC1 upregulation and prevented podocyte injury. The current study demonstrated that overexpression of miR‑126 could protect podocytes from sepsis‑induced injury through an EGFL6/DKC1 signaling pathway.Branched chain amino acid transaminase 1 (BCAT1) overexpression has been reported in various cancers; however, at present, its significance and biological role in head and neck squamous cell carcinoma (HNSCC) remain unknown. BCAT1 protein expression was upregulated in 56/106 (52.8%) cases of HNSCC. BCAT1 overexpression was associated with tumor‑node‑metastasis stage, tumor stage and nodal metastasis. The Cancer Genome Atlas data suggested that high BCAT1 expression was associated with poor patient survival. Oncomine data suggested that BCAT1 expression was increased in HNSCC. Functionally, BCAT1 overexpression promoted cell proliferation, colony formation, invasion and cisplatin resistance in FaDu cells. BCAT1 overexpression also upregulated the mitochondrial membrane potential, and increased ATP production, glucose consumption and glucose uptake. Western blotting demonstrated that BCAT1 overexpression upregulated c‑Myc and glucose transporter 1 (GLUT1) protein levels. Depletion of c‑Myc using small interfering RNA abolished the influence of BCAT1 on GLUT1. Chromatin immunoprecipitation assays demonstrated that c‑Myc has binding sites in the GLUT1 promoter. Collectively, the present findings suggested that BCAT1 is upregulated in human HNSCC and regulates HNSCC cell proliferation, invasion, cisplatin sensitivity and c‑Myc/GLUT1 signaling.With‑no‑lysine kinase 3 (WNK3) is a serine/threonine kinase that functions by regulating downstream signaling molecules. WNK3 mainly regulates intracellular and extracellular Na+, Cl‑ and K+ levels by regulating downstream ion transporters, the disruption of which has been associated with cerebral ischemia, epilepsy, glioma and other diseases. In addition, WNK3 was demonstrated to regulate neuronal splicing factor RNA binding fox‑1 homolog‑1 to influence autism. Over the past 20 years, accumulating evidence has reported that dysfunctional WNK3 signaling was involved in the pathologies of various neurological disorders; therefore, WNK3 has become a promising therapeutic target for ameliorating the corresponding symptoms of such disorders. The present review aimed to provide a general overview of the expression patterns and physiological functions of WNK3 signaling and its pathophysiological roles in neurological diseases, such as epilepsy, ischemic brain injury, intracerebral hemorrhage, autism, glioma and schizophrenia.Circular RNA ABCB10 (circ‑ABCB10) modulates cellular functions and microRNA (miR)‑1271 in epithelial ovarian cancer (EOC). The present study aimed to investigate the interaction between circ‑ABCB10 and miR‑1271 in regulating EOC cellular function and the calpain small subunit 1 (Capn4)/Wnt/β‑catenin signaling pathway. circ‑ABCB10 and miR‑1271 expression levels were detected in EOC cells (OVCAR3, UWB1.289, SKOV3 and CAOV3) and normal ovarian epithelial cells (IOSE80) via reverse‑transcription quantitative PCR. SKOV3 cells were transfected with control short hairpin (sh)RNA plasmids, control inhibitor, circ‑ABCB10 shRNA plasmids and miR‑1271 inhibitor. UWB1.289 cells were transfected with control overexpression plasmids, control mimic, circ‑ABCB10 overexpression plasmids and miR‑1271 mimic. Subsequently, cell proliferation, apoptosis, invasion and the Capn4/Wnt/β‑catenin signaling pathway were assessed. In addition, a luciferase activity assay was performed. circ‑ABCB10 expression was significantly increased inion, and suppressed apoptosis by regulating the miR‑1271‑mediated Capn4/Wnt/β‑catenin signaling pathway in EOC.