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Background: Exportin 1 (XPO1) is a nuclear export protein that facilitates the transportation of various substances. XPO1 promotes tumor development as a poor prognostic factor in a variety of tumors and is a therapeutic target for screening inhibitors. However, the role of XPO1 in oral squamous cell carcinoma (OSCC) has yet to be determined. Methods: The expression patterns of XPO1 mRNA in OSCC were investigated using bioinformatics tools, and the expression levels of XPO1 protein in OSCC specimens were confirmed by immunohistochemical assays. Survival analysis was conducted to evaluate the impact of XPO1 on prognosis. GO and KEGG enrichment analyses were utilized to uncover the signaling pathways mediated by XPO1. Additionally, we examined the association between XPO1 and AKT/MAPK/TGFBR1 and immune infiltration. Results: XPO1 mRNA and protein expression levels were significantly enhanced in OSCC and associated with OSCC severity. Enhanced XPO1 expression was indicative of poor survival. Functional analysis showed that XPO1 mediated pathways associated with cell cycle and DNA replication and reduced immune infiltration in OSCC. Additionally, XPO1 mRNA and protein expression levels had significant positive relationships with AKT/MAPK/TGFBR1. Conclusions: XPO1, as a marker of poor prognosis in OSCC, can promote OSCC through AKT/MAPK/TGFBR1. [ABSTRACT FROM AUTHOR]

Inadequate reference databases in RNA-seq analysis can hinder data utilization and interpretation. In this study, we have successfully constructed a high-quality reference transcript dataset, ZjRTD1.0, for Zoysia japonica, a widely-used turfgrass with exceptional tolerance to various abiotic stress, including low temperatures and salinity. This dataset comprises 113,089 transcripts from 57,143 genes. BUSCO analysis demonstrates exceptional completeness (92.4%) in ZjRTD1.0, with reduced proportions of fragmented (3.3%) and missing (4.3%) orthologs compared to prior datasets. ZjRTD1.0 enables more precise analyses, including transcript quantification and alternative splicing assessments using public datasets, which identified a substantial number of differentially expressed transcripts (DETs) and differential alternative splicing (DAS) events, leading to several novel findings on Z. japonica's responses to abiotic stresses. First, spliceosome gene expression influenced alternative splicing significantly under abiotic stress, with a greater impact observed during lowtemperature stress. Then, a significant positive correlation was found between the number of differentially expressed genes (DEGs) encoding protein kinases and the frequency of DAS events, suggesting the role of protein phosphorylation in regulating alternative splicing. Additionally, our results suggest possible involvement of serine/arginine-rich (SR) proteins and heterogeneous nuclear ribonucleoproteins (hnRNPs) in generating inclusion/exclusion isoforms under low-temperature stress. Furthermore, our investigation revealed a significantly enhanced overlap between DEGs and differentially alternatively spliced genes (DASGs) in response to lowtemperature stress, suggesting a unique co-regulatory mechanism governing transcription and splicing in the context of low-temperature response. In conclusion, we have proven that ZjRTD1.0 will serve as a reliable and useful resource for future transcriptomic analyses in Z. japonica. [ABSTRACT FROM AUTHOR]

Aim: Enhanced cardiac sympathetic afferent reflex (CSAR) promotes sympathetic hyperactivation in chronic heart failure (CHF). Salusin‐β is a torsin family 2 member A (TOR2A) gene product and a cardiovascular active peptide closely associated with cardiovascular diseases. We aimed to determine the roles of salusin‐β in the paraventricular nucleus (PVN) in modulating enhanced CSAR and sympathetic hyperactivation in rats with CHF induced by coronary artery ligation and elucidate the underlying molecular mechanisms. Methods: CSAR was evaluated based on the responses of mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) to the epicardial administration of capsaicin in rats under anesthesia. Results: Salusin‐β protein expression was upregulated in the PVN of the CHF compared with sham‐operated rats. Salusin‐β microinjection into the PVN dose‐dependently increased MAP and RSNA and enhanced CSAR, while anti‐salusin‐β IgG exerted opposite effects. The effect of salusin‐β was inhibited by reactive oxygen species (ROS) scavenger or NAD(P)H oxidase inhibitor but promoted by superoxide dismutase inhibitor. The effect of anti‐salusin‐β IgG was interdicted by nitric oxide (NO) synthase inhibitor. Furthermore, chronic salusin‐β gene knockdown in PVN attenuated CSAR, reduced sympathetic output, improved myocardial remodeling and cardiac function, decreased NAD(P)H oxidase activity and ROS levels, and increased NO levels in the CHF rats. Conclusion: Increased salusin‐β activity in the PVN contributes to sympathetic hyperactivation and CSAR in CHF by inhibiting NO release and stimulating NAD(P)H oxidase‐ROS production. Reducing endogenous central salusin‐β expression might be a novel strategy for preventing and treating CHF in the future. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to investigate the role and related mechanism of chordin‐like 1 (CHRDL1) in oral squamous cell carcinoma (OSCC). Methods: The expressions of CHRDL1 were analyzed in both mRNA and protein levels by bioinformatics analysis, immunohistochemistry, and fluorescence in situ hybridization in OSCC. Survival analysis was used to determine the relationship between CHRDL1 and prognosis. In addition, enrichment analysis was used to suggest signal pathways involved in CHRDL1. Besides, the relationships between CHRDL1 and miRNAs, hypoxia, and immune infiltration were explored. Results: The mRNA level of CHRDL1 in OSCC was significantly lower than that in normal tissues, while the protein level was significantly higher than that in normal tissues. The high mRNA levels of CHRDL1 suggested a poor prognosis in patients with OSCC. The enrichment results showed that CHRDL1 might be involved in the Calcium signaling pathway, dilated cardiomyopathy, and focal adhesion. 7 immune cells were positively correlated with CHRDL1, while Tgd was negatively correlated with CHRDL1. In addition, we also found that hsa‐miR‐455‐3p directly targeted CHRDL1 and reduced the mRNA levels of CHRDL1. Conclusion: CHRDL1 plays a vital role in promoting cancer in OSCC and is down‐regulated at the mRNA levels by hsa‐miR‐455‐3p. [ABSTRACT FROM AUTHOR]

Aim: To ascertain the anti‐inflammation mechanism of catechins in lipopolysaccharide‐treated human dental pulp cells (HDPCs). Methods: Expression of tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, and IL‐6 was measured using quantitative polymerase chain reaction (qPCR) and enzyme‐linked immunosorbent assays. The anti‐inflammatory mechanism was explored by examining activation of nuclear factor‐kappa B (NF‐κB) signaling using qPCR, Western blotting, and immunofluorescence staining. Results: Human dental pulp cells proliferation was not affected by treatment with epigallocatechin (ECG) or epigallocatechin 3‐gallate (EGCG). mRNA expression of the pro‐inflammatory cytokines TNF‐α, IL‐1β, and IL‐6 was decreased significantly in ECG‐ and EGCG‐treated HDPCs. Subsequently, the effects of ECG and EGCG upon activation of NF‐κB signaling were evaluated by Western blotting and immunofluorescence staining. Expression of p‐p65 protein in HDPCs treated with ECG, EGCG, or an NF‐κB inhibitor (Bay 11‐7082) was lower than that in HDPCs treated with lipopolysaccharide, data that were consistent with the location of p65 protein according to immunofluorescence staining. Conclusions: Catechin could reduce lipopolysaccharide‐stimulated inflammation in HDPCs by inhibiting activation of the NF‐κB pathway. [ABSTRACT FROM AUTHOR]

MicroRNAs are small non-coding RNA molecules that control expression of target genes. Previous studies showed that microRNA-107 (miR-107) is overexpressed in gastric cancer tissues compared with the matched normal tissues. However, it remains largely unclear as to how miR-107 exerts its function and modulates the malignant phenotypes of gastric cancer, because our understanding of miR-107 signalling pathways is limited. In this study, we demonstrate that miR-107 is frequently up-regulated in gastric cancers and its overexpression is significantly associated with gastric cancer metastasis. Furthermore, silencing the expression of miR-107 could inhibit gastric cancer cell migration and invasion in vitro and in vivo. Subsequent investigation characterized DICER1 as a direct target of miR-107. Up-regulation of DICER1 resulted in a dramatic reduction of in vitro migration, invasion, in vivo liver metastasis of nude mice, which is similar to that occurs with the silencing of miR-107, indicating that DICER1 functions as a metastasis suppressor in gastric cancer. Furthermore, the restoration of DICER1 can inhibit miR-107-induced gastric cancer cell invasion and metastasis. In conclusion, our results suggested that miR-107, an oncogene miRNA promoting gastric cancer metastasis through down-regulation of DICER1. Inhibition of miR-107 or restoration of DICER1 may represent a new potential therapeutic target for gastric cancer treatment. [ABSTRACT FROM AUTHOR]