Joynernymand4533

Human cathelicidin antimicrobial peptide and its active product, LL‑37 (CAMP/LL‑37), exhibit a broad spectrum of antimicrobial effects. An increasing number of studies have shown that human CAMP/LL‑37 also serves significant roles in various types of cancer. The primary aims of the present study were to investigate the roles and mechanisms of human CAMP/LL‑37 in oral squamous cell carcinoma (OSCC) cells. The results indicated that either LL‑37 C‑terminal deletion mutants (CDEL) or CAMP stable expression in HSC‑3 cells reduced colony formation, proliferation, migration and invasion ability of the cells. Expression analysis demonstrated that either CDEL or CAMP stable expression in HSC‑3 cells induced caspase‑3 mediated apoptosis via the P53‑Bcl‑2/BAX signalling pathway, whereas the levels of cell cycle‑related proteins, cyclin B1 and PKR‑like ER kinase, were significantly upregulated in the CAMP, but not in the CDEL overexpressing cells. Transcriptional profile comparisons revealed that CDEL or CAMP stable expression in HSC‑3 cells upregulated expression of genes involved in the IL‑17‑dependent pathway compared with the control. Taken together, these results suggest that CAMP may act as a tumour suppressor in OSCC cells, and the underlying mechanism involves the induction of caspase‑3 mediated apoptosis via the P53‑Bcl‑2/BAX signalling pathway.Abnormal menstruation may result in several pathological alterations and gynaecological diseases, including endometriosis, menstrual pain and miscarriage. However, the pathogenesis of menstruation remains unclear due to the limited number of animal models available to study the menstrual cycle. In recent years, an effective, reproducible, and highly adaptive mouse model to study menstruation has been developed. Enitociclib In this model, progesterone and oestrogen were administered in cycles following the removal of ovaries. Subsequently, endometrial decidualisation was induced using sesame oil, followed by withdrawal of progesterone administration. Vaginal bleeding in mice is similar to that in humans. Therefore, the use of mice as a model organism to study the mechanism of menstruation and gynaecological diseases may prove to be an important breakthrough. The present review is focussed ond the development and applications of a mouse model of menstruation. Furthermore, various studies have been described to improve this model and the research findings that may aid in the treatment of menstrual disorders in women are presented.Hypertrophic scars (HSs) are a progressive fibroproliferation disorder caused by abnormal tissue repair after deep skin injury, and are characterized by continuous activation of fibroblasts and excessive deposition of extracellular matrix. Arctigenin (ATG), a phytomedicine derived from certain plants, displays antifibrotic effects in certain diseases, such as oral submucous fibrosis and peritoneal fibrosis. In the present study, to determine the antifibrotic potential of ATG in HS, a bleomycin (BLM)‑induced skin fibrosis murine model was established. C57BL/6 mice were randomly divided into Control group, BLM group and BLM+ATG group. At 1 day post‑bleomycin induction, the BLM+ATG group was intraperitoneally injected with 3 mg/kg/day ATG for 28 consecutive days. Pathological changes in the skin tissues were observed by hematoxylin and eosin staining. Collagen content was determined using a Sircol Collagen assay kit. Immunofluorescence staining was performed to detect the expression of TGF‑β1 and α‑SMA. The expr of oxidants (malondialdehyde) in the BLM+ATG group compared with the BLM group. Moreover, the results indicated that the antioxidant effect of ATG may occur via activation of the nuclear factor erythroid‑2‑related factor 2/heme oxygenase‑1 signaling pathway. Collectively, the present study indicated that ATG could ameliorate skin fibrosis in a murine model of HS, which was partly mediated by reducing inflammation and oxidative stress. Therefore, ATG may serve as a therapeutic agent for HSs.ETS variant 1 (ETV1) is an oncogenic transcription factor. However, its role in colorectal cancer has remained understudied. The present study demonstrated that ETV1 downregulation led to reduced HCT116 colorectal cancer cell growth and clonogenic activity. Furthermore, the ETV1 mRNA levels were enhanced in colorectal tumors and were associated with disease severity. In addition, ETV1 directly bound to Jumonji C domain‑containing (JMJD) 1A, a histone demethylase known to promote colon cancer. ETV1 and JMJD1A, but not a catalytically inactive mutant thereof, cooperated in inducing the matrix metalloproteinase (MMP)1 gene promoter that was similar to the cooperation between ETV1 and another histone demethylase, JMJD2A. RNA‑sequencing revealed multiple potential ETV1 target genes in HCT116 cells, including the FOXQ1 and TBX6 transcription factor genes. Moreover, JMJD1A co‑regulated FOXQ1 and other ETV1 target genes, but not TBX6, whereas JMJD2A downregulation had no impact on FOXQ1 as well as TBX6 transcription. Accordingly, the FOXQ1 gene promoter was stimulated by ETV1 and JMJD1A in a cooperative manner, and both ETV1 and JMJD1A bound to the FOXQ1 promoter. Notably, the overexpression of FOXQ1 partially reversed the growth inhibitory effects of ETV1 ablation on HCT116 cells, whereas TBX6 impaired HCT116 cell growth and may thereby dampen the oncogenic activity of ETV1. The latter also revealed for the first time, to the best of our knowledge, a potential tumor suppressive function of TBX6. Taken together, the present study uncovered a ETV1/JMJD1A‑FOXQ1 axis that may drive colorectal tumorigenesis.Mulberry leaves have antioxidant activity and anti‑inflammatory effects in several types of cells. However, the efficacy of mulberry leaves fermented with Cordyceps militaris remains unknown. Therefore, the present study aimed to investigate whether the ethanol extracts of mulberry leaves fermented with C. militaris (EMfC) can prevent lipopolysaccharide (LPS)‑induced inflammation and autophagy in macrophages. link2 To achieve this, RAW264.7 cells pretreated with three different dose of EMfCs were subsequently stimulated with LPS, and examined for alterations in the regulatory factors of inflammatory responses and key parameters of the autophagy signaling pathway. EMfC treatment inhibited the generation of reactive oxidative species; however, significant activity was observed for 2,2‑diphenyl‑1‑picrylhydrazyl (DPPH) radical scavenging (IC50=579.6703 mg/ml). Most regulatory factors in inflammatory responses were significantly inhibited following treatment with EMfC, without any significant cellular toxicity. EMfC‑treated groups exhibited marked suppression of nitrogen oxide (NO) levels, mRNA expression levels of iNOS/COX‑2, levels of all inflammatory cytokines (TNF‑α, IL‑1β and IL‑6) and phosphorylation of MAPK members, as well as recovery of cell cycle progression. Furthermore, similar effects were observed in the LPS‑induced autophagy signaling pathway of RAW264.7 cells. The expression levels of microtubule‑associated protein 1A/1B‑light chain 3 (LC3) and Beclin exhibited a dose‑dependent decrease in the EMfC+LPS‑treated groups compared with in the Vehicle+LPS‑treated group, whereas the phosphorylation of PI3K and mTOR were enhanced in a dose‑dependent manner in the same groups. Overall, the results of the present study provide evidence that exposure to EMfC protects against LPS‑induced inflammation and autophagy in RAW264.7 cells. These results indicated that EMfC is a potential candidate for treatment of inflammatory diseases.The human ocular surface produces highly conserved cationic peptides. Human β‑defensins (HBDs) serve an important role in innate and adaptive immunity. They are primarily expressed in epithelial cells in response to infection and provide the first line of defence against invading microbes. Defensin β1 (DEFB1) is constitutively expressed and regulated by inflammatory mediators including interferon‑γ, lipopolysaccharide and peptidoglycans. DEFB4A is locally induced in response to microbial infection while DEFB109 is induced via Toll‑like receptor 2. The present study examined the expression of the HBD DEFB1, DEFB4A and DEFB109 genes in pterygium. The pterygium tissues and normal conjunctiva samples were obtained from 18 patients undergoing pterygium surgery. The reverse transcription‑quantitative polymerase chain reaction method was employed to determine the expression of DEFB1, DEFB4A and DEFB109 genes. The results revealed that the expression of DEFB1 and DEFB4A was significantly higher and upregulated in pterygium samples when compared with normal conjunctiva samples from each patient (P less then 0.05), while the expression of DEFB109 was observed to be lower in pterygium samples when compared with normal samples from the same patient. Previous studies have revealed that DEFB1 and DEFB4A genes are present in low concentrations inside the human eye, and they are upregulated during the maturation of keratinocytes, suggesting a possible role in cell differentiation. The DEFB109 gene is present in higher concentrations inside the human eye, though it is newly discovered. It has also been reported that DEFB1 may be involved in carcinogenesis epithelial tumours. Collectively, the current data suggests that HBDs may serve a crucial role in the pathogenesis and development of pterygia, and thus may be considered as novel molecular targets in understanding pterygia development.Hypertrophic cardiomyopathy (HCM) is one of the most commonly inherited heart diseases and the leading cause of sudden cardiac death among adolescents and young adults. Circulating long noncoding RNAs (lncRNAs) have demonstrated potential as diagnostic and therapeutic targets in several cardiovascular diseases. link3 However, the circulating extracellular lncRNA expression profile of patients with HCM remains unclear. Plasma lncRNA expression was evaluated in patients with HCM and healthy controls using a human lncRNA microarray. A weighted correlation network analysis (WGCNA) and linear models for microarray data (Limma) were used. GSE68316 data from cardiac tissue in the Gene Expression Omnibus database were analysed for further validation. Using WGCNA, two modules (referred to as the magenta and the light‑yellow module) were identified that were positively associated with HCM. Gene Ontology analysis revealed that lncRNAs in the magenta module targeted 'heart growth'. Using Limma, a total of 290 lncRNAs were differentially expressed (210 upregulated and 80 downregulated) in the plasma of HCM patients, compared with controls. Moreover, combined WGCNA and Limma analysis demonstrated that 27 hub lncRNAs in the magenta module and 13 hub lncRNAs in the light‑yellow module were significantly upregulated, compared with the controls. Moreover, of the 40 differentially expressed hub lncRNAs identified in the two modules, three circulating lncRNAs (lnc‑P2RY6‑11, ENST00000488040 and ENST00000588047) were also significantly upregulated in the HCM cardiac tissue validation dataset. These lncRNAs may serve as biomarkers and therapeutic targets for precise diagnosis and treatment of HCM.