Ruizgoode2992

The area under the curve for miR‑25‑3p in the diagnosis of breast cancer was 0.748, with 57.1% sensitivity and 95.0% specificity. Moreover, the Kaplan‑Meier survival curves demonstrated that patients with breast cancer with a low expression of serum miR‑25‑3p had a higher overall survival rate compared with patients with a high serum miR‑25‑3p expression. miR‑25‑3p knockdown suppressed breast cancer cell proliferation and invasion, and transducer of ERBB2, 1 (TOB1) was identified as a potential target gene regulated by miR‑25‑3p. Therefore, the present study suggested that miR‑25‑3p regulated cellular functions via TOB1 in breast cancer; therefore, miR‑25‑3p may serve as a breast cancer biomarker.Circular RNAs (circRNAs) are a class of non‑coding RNAs with a circular, covalent structure that lack both 5' ends and 3' poly(A) tails, which are stable and specific molecules that exist in eukaryotic cells and are highly conserved. The role of circRNAs in viral infections is being increasingly acknowledged, since circRNAs have been discovered to be involved in several viral infections (such as hepatitis B virus infection and human papilloma virus infection) through a range of circRNA/microRNA/mRNA regulatory axes. These findings have prompted investigations into the potential of circRNAs as targets for the diagnosis and treatment of viral infection‑related diseases. The aim of the present review was to systematically examine and discuss the role of circRNAs in several common viral infections, as well as their potential as diagnostic markers and therapeutic targets.As an important type of programmed cell death in addition to apoptosis, necroptosis occurs in a variety of pathophysiological processes, including infections, liver diseases, kidney injury, neurodegenerative diseases, cardiovascular diseases, and human tumors. It can be triggered by a variety of factors, such as tumor necrosis factor receptor and Toll‑like receptor families, intracellular DNA and RNA sensors, and interferon, and is mainly mediated by receptor‑interacting protein kinase 1 (RIP1), RIP3, and mixed lineage kinase domain‑like protein. A better understanding of the mechanism of necroptosis may be useful in the development of novel drugs for necroptosis‑related diseases. In this review, the focus is on the molecular mechanisms of necroptosis, exploring the role of necroptosis in different pathologies, discussing their potential as a novel therapeutic target for disease therapy, and providing suggestions for further study in this area.Cerebral ischemia‑reperfusion injury (CIRI) refers to the phenomenon that ischemic injury of the brain leads to the injury of brain cells, which is further aggravated after the recovery of blood reperfusion. Dihydromyricetin (DHM) has an effective therapeutic effect on vascular diseases; however, its role in CIRI has not been investigated. The oxygen and glucose deprivation/reoxygenation (OGD/R) cell model was used on HT22 hippocampal neurons in mice, by oxygen and sugar deprivation. DHM was found to increase the cell viability of HT22 cells following OGD/R induction. The levels of malondialdehyde (MDA) decreased, superoxide dismutase (SOD) and glutathione (GSH) in the OGD/R‑induced HT22 cells increased following DHM treatment, accompanied by the decreased protein expression levels of NOX2 and NOX4. Relacorilant antagonist DHM also inhibited cell apoptosis induced by OGD/R, and decreased the protein expression levels of Bax and caspase‑3, and increased the expression levels of Bcl‑2. Moreover, the expression levels of the NF‑E2‑related factor 2 (Nrf2)/heme oxygenase (HO‑1) signaling pathway‑associated proteins in OGD/R‑induced HT22 were increased following DHM treatment, and the effect of DHM on oxidative stress and apoptosis was reversed after the addition of the Nrf2/HO‑1 pathway inhibitor, brusatol. In conclusion, DHM inhibited oxidative stress and apoptosis in OGD/R‑induced HT22 cells by activating the Nrf2/HO‑1 signaling pathway.Disruption in mucins (MUCs) is involved in cancer development and metastasis and is thus used as a biomarker. Non‑small cell lung carcinoma (NSCLC) is characterized by heterogeneous genetic and epigenetic alterations. Lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC) are the two primary subtypes of NSCLC that require different therapeutic interventions. Here, we report distinct expression and epigenetic alterations in mucin 22 (MUC22), a new MUC family member, in LUSC vs. LUAD. In lung cancer cell lines and tissues, MUC22 was downregulated in LUSC (MUC22Low) but upregulated in LUAD (MUC22High) with co‑expression of MUC21. The aberrant expression of MUC22 was inversely correlated with its promoter hypermethylation in LUSC and hypomethylation in LUAD cells and tissues, respectively. Decreased MUC22 expression in NSCLC cell lines was restored upon treatment with epigenetic modifiers 5‑aza‑2'‑deoxycytidine (5‑Aza) or trichostatin A (TSA), accompanied by reduction in global protein level of histone deacetylase 1 (HDAC1) but increased enrichment of histone H3 lysine 9 acetylation (H3K9ac) specifically in the MUC22 promoter in the SK‑MES‑1 cell line. MUC22 knockdown increased the growth and motility of lung cancer cells and an immortalized human bronchial epithelial BEAS‑2B cell line via NF‑κB activation. Clinically, MUC22Low in LUSC and MUC22High in LUAD were shown to be indicators of unfavorable overall survival for patients with early cancer stages. Our study reveals that changes in MUC22 expression due to epigenetic alterations in NSCLC may have important biological significance and prognostic potential in LUSC when compared to LUAD. Thus, MUC22 expression and epigenetic alterations may be used for molecular subtyping of NSCLC in precision medicine.Cervical cancer is a common public health issue with high morbidity worldwide. Paeonol (Pae) has been recognized as a traditional Chinese medicine used for the treatment of various cancer types. However, whether Pae could exert a protective effect on cervical cancer remains to be investigated. The aim of the present study was to explore the role of Pae in cervical cancer cells and identify the potential mechanism. Cell Counting Kit‑8 and colony‑formation assays were conducted to test the proliferation of HeLa cells. Additionally, wound healing and transwell assays were used to detect the migratory and invasive abilities of cells. The plasmid that overexpressed 5‑lipoxygenase (5‑LO) or control vector was constructed and transfected into the cells. Subsequently, flow cytometry was used to monitor the apoptotic rate of cells. The expression levels of apoptosis‑associated proteins and 5‑LO were detected using western blot analysis. Reverse transcription‑quantitative PCR analysis detected the expression of 5‑LO. Pae inhibited the proliferation, invasion and migration of HeLa cells, promoted cell apoptosis and downregulated the expression of 5‑LO.