GSTO1 overexpression also significantly increased the phosphorylation levels of JAK and STAT3, whereas the knockdown of GSTO1 promoted the opposite effects. In conclusion, the findings of the present study indicated that GSTO1 may serve as an oncogene in NSCLC. The results suggested that GSTO1 may have an important role in NSCLC by regulating the JAK/STAT3 signaling pathway. Therefore, inhibiting the expression levels of GSTO1 may represent a potential novel therapeutic strategy for NSCLC.Through searching for anti‑neuroinflammatory metabolites from Nardostachys jatamansi extracts, nardostachin was revealed to exert anti‑neuroinflammatory effects against lipopolysaccharide (LPS)‑induced overproduction of nitric oxide and prostaglandin E2 in BV2 and rat primary microglial cells. Furthermore, nardostachin inhibited the production of inducible nitric oxide synthase and cyclooxygenase‑2 as well as pro‑inflammatory cytokines, including interleukin (IL)‑1β, IL‑6, IL‑12 and tumor necrosis factor‑α in LPS‑stimulated BV2 and rat primary microglial cells. In a mechanistic study, nardostachin exhibited inhibitory activity on the nuclear factor (NF)‑κB signaling pathway in LPS‑stimulated BV2 and rat primary microglial cells by repressing IκB‑α phosphorylation and blocking NF‑κB translocation. Furthermore, nardostachin exhibited inhibitory effects on LPS‑induced phosphorylation of c‑Jun N‑terminal kinase (JNK) mitogen‑activated protein kinase (MAPK). Additionally, nardostachin repressed protein expression of Toll‑like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) in LPS‑induced BV2 and rat primary microglial cells. These results suggested that nardostachin exerts anti‑neuroinflammatory effects on LPS‑induced BV2 and rat primary microglial cells by suppressing the TLR4‑MyD88‑NF‑κB and JNK MAPK pathways.Loss‑of‑function BRCA mutations are frequent in high‑grade serous ovarian carcinoma. BRCA1 and ‑2 mutations lead to homologous recombination (HR) deficiency. Poly(ADP‑ribose) polymerases (PARP) are enzymes involved in DNA repair. PARP inhibitors (PARPi) lead to DNA damage accumulation in cells deficient in HR. Olaparib (a PARPi) is currently used for the treatment of high‑grade serous ovarian carcinoma with germline or somatic BRCA mutations; however, numerous patients do not respond or eventually develop resistance to these agents. The TP53 gene encodes the p53 protein, which is often referred to as the 'guardian of the genome'. TP53 mutations at diagnosis are known to promote resistance to chemotherapy. In the present study, four cases of patients with BRCA‑mutated cancer treated with olaparib, who progressed following the PARPi treatment, are reported. Exome analyses were performed on a primary tumor biopsy at diagnosis, then on a progressing metastasis following olaparib treatment. Exome analyses following olaparib treatment identified de novo TP53 mutations, as well as increased frequencies of pre‑existing TP53 mutations compared with the primary tumor. In HCT116 TP53‑/‑ cells carrying BRCA2 pathogenic mutations, TP53 inactivating mutations were associated with lower sensitivity to olaparib in vitro. find more Thus, inactivating TP53 mutations may be associated to olaparib resistance in the presence of BRCA mutations. In conclusion, the present findings demonstrated resistance to PARPi with de novo TP53 mutations that may be clinically relevant. As TP53 mutations are easily detectable with targeted next‑generation sequencing panels, these may serve as surrogate markers for the onset of PARPi resistance in the context of routine patient management strategies.Resveratrol confers neuroprotective effects in cerebral ischemia; however, the involvement of mitophagy in the neuroprotective function of resveratrol remains unclear. The aim of the present study was to investigate whether resveratrol exerts neuroprotective effects on primary cortical neurons subjected to oxygen/glucose deprivation/reoxygenation (OGD/R) via modulating mitophagy. The data demonstrated that resveratrol at 1‑10 µM during reoxygenation improved cell viability and suppressed apoptosis following OGD/R in a concentration‑dependent manner. Moreover, resveratrol alleviated OGD/R‑induced loss of mitochondrial membrane potential and excessive oxidative stress. Confocal imaging of LC3 and TOM20 antibody‑labeled mitochondria, as well as western blot analysis, demonstrated that mitophagy was further enhanced following resveratrol treatment. In addition, resveratrol was revealed to stimulate the phosphatase and tensin homolog‑induced kinase 1/Parkin pathway. Mitophagy inhibition then inhibited the protective effects of resveratrol. These results indicated that resveratrol exerts its protective effects against OGD/R damage, at least in part, by promoting mitophagy.Long non‑coding (lnc)RNAs and microRNAs (miRNAs/miRs) have physiological and pathological functions in various diseases, including gastric cancer (GC). The current study explored the association between lncRNA small nucleolar RNA host gene 4 (SNHG4) and miR‑148a‑3p, and their functions in GC cells. SNHG4 expression and overall survival data were analyzed using bioinformatics, and the interaction of SNHG4 and miR‑148a‑3p was predicted using starBase and confirmed via a dual‑luciferase reporter assay. Cell viability, colony formation ability and apoptosis rate were detected using Cell Counting Kit‑8, colony formation and flow cytometry assays, respectively. Cell migration and invasion were determined via wound‑healing and Transwell assays. mRNA and protein expression levels were determined via reverse transcription‑quantitative PCR and western blotting. The results demonstrated that in GC tissues and cell lines, SNHG4 was highly expressed, while miR‑204‑5p expression was decreased, and that the expression levels of SNHG4 and miR‑204‑5p were negatively correlated. The downregulated expression of SNHG4 decreased the effects of miR‑204‑5p inhibitor on promoting cell proliferation, migration, invasion and epithelial‑mesenchymal transition, but enhanced the inhibitory effect of miR‑204‑5p on GC cell apoptosis. The findings of the current study revealed the potential mechanism of the SNHG4‑miR‑204‑5p pathway in GC, which may be conducive to the development of novel drugs against GC growth.