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In this study, effects of continuous cropping on soil properties, enzyme activities, and relative abundance, community composition and diversity of fungal taxa were investigated. Rhizosphere soil from field continuously cropped for one-year, three-year and five-year by Coptis chinensis Franch. was collected and analyzed. Illumina high-throughput sequencing analysis showed that continuous cropping of C. chinensis resulted in a significant and continuous decline in the richness and diversity of soil fungal population. Ascomycota, Zygomycota, Basidiomycota, and Glomeromycota were the dominant phyla of fungi detected in rhizosphere soil. Fungal genera such as Phoma, Volutella, Pachycudonia, Heterodermia, Gibberella, Cladosporium, Trichocladium, and Sporothrix, were more dominant in continuously cropped samples for three-year and five-year compared to that for one-year. By contrast, genera, such as Zygosaccharomyces, Pseudotaeniolina, Hydnum, Umbelopsis, Humicola, Crustoderma, Psilocybe, Coralloidiomyces, Mortierella, Polyporus, Pyrenula, and Monographella showed higher relative abundance in one-year samples than that in three-year and five-year samples. Cluster analysis of the fungal communities from three samples of rhizosphere soil from C. chinensis field revealed that the fungal community composition, diversity, and structure were significantly affected by the continuous cropping. Continuous cropping of C. chinensis also led to significant declines in soil pH, urease, and catalase activities. Redundancy analysis showed that the soil pH had the most significant effect on soil fungal population under continuous cropping of C. chinensis.

Background Suicide among university students in China constitutes a critical public health challenge. Although numerous studies have examined risk factors, most have relied on cross-sectional designs. Evidence from longitudinal studies, particularly regarding protective factors, remains limited. This systematic review and meta-analysis synthesizes longitudinal evidence to identify risk and protective factors for suicidal ideation and suicide attempts among Chinese university students. Methods Six electronic databases (three English-language and three Chinese-language databases) were systematically searched for longitudinal studies published up to October 2024. Eligible studies investigated predictors of suicidal ideation or suicide attempts among Chinese university students. Random-effects meta-analyses were conducted to estimate pooled effect sizes, expressed as odds ratios (ORs). Meta-regression analyses were used to examine temporal moderators, and heterogeneity and publication bias were assessed. Results Twenty-two longitudinal studies comprising 953,651 participants were included. The strongest predictors of subsequent suicidal ideation were prior suicidal ideation, anxiety, and early morning awakening. Suicide attempts were most strongly associated with prior non-suicidal self-injury, insomnia symptoms, and academic pressure. Higher levels of social support were associated with a reduced risk of suicidal ideation, whereas other examined protective factors were not statistically significant. Meta-regression analyses indicated that the predictive strength of depressive symptoms for suicidal ideation attenuated with longer follow-up periods. Conclusions Sleep disturbances, academic pressure, and prior suicidal ideation may represent important targets for early identification among Chinese university students. The findings highlight the importance of addressing both psychological vulnerabilities and contextual stressors in suicide prevention efforts. Future longitudinal research should adopt standardized measurements to enhance comparability and inform culturally tailored population-level prevention strategies.

Limiting purine intake, inhibiting xanthine oxidoreductase (XOR) and inhibiting urate reabsorption in proximal tubule by uricosuric drugs, to reduce serum uric acid (UA) levels, are recognized treatments for gout. However, the mechanism of increased how XOR expression and activity in hyperuricemia and gout remains unclear. This study aims to explore whether exogenous purines are responsible for increased XOR expression and activity. HepG2 and Bel-7402 human hepatoma cells were stimulated with exogenous purine, or were exposed to conditioned growth medium of purine-stimulated Jurkat cells, followed by measurement of XOR expression and UA production to determine the effect of lymphocyte-secreted cytokines on XOR expression in hepatocytes. The expression of STAT1, IRF1 and CBP and their binding on the promoter were detected by western blotting and ChIP-qPCR. The level of DNA methylation was determined by bisulfite sequencing PCR. Blood samples from 117 hyperuricemia patients and 119 healthy individuals were collected to analyze the correlation between purine, UA and IFN-γ concentrations. Excess of purine was metabolized to UA in hepatocyte metabolism by XOR that was induced by IFN-γ secreted in the conditioned growth medium of Jurkat cells in response to exogenous purine, but it did not directly induce XOR expression. IFN-γ upregulated XOR expression due to the enhanced binding of STAT1 to IRF1 to further recruit CBP to the promoter. Clinical data showed positive correlation of serum IFN-γ with both purine and UA, and associated risk of hyperuricemia. Purine not only acts as a metabolic substrate of XOR for UA production, but it induces inflammation through IFN-γ secretion that stimulates UA production through elevation of XOR expression.

The human DHRS4 gene cluster consists of DHRS4 and two immediately downstream homologous genes, DHRS4L2 and DHRS4L1 , generated by evolutionarily gene-duplication events. We previously demonstrated that a head-to-head natural antisense transcript (NAT) of DHRS4 , denoted DHRS4-AS1 , regulates all three genes of the DHRS4 gene cluster. However, it is puzzling that DHRS4L2 and DHRS4L1 did not evolve their own specific NATs to regulate themselves, as it seems both have retained sequences highly homologous to DHRS4-AS1 . In a search of the DHRS4-AS1 region for nearby enhancers, we identified an enhancer located 13.8 kb downstream of the DHRS4-AS1 transcriptional start site. We further showed, by using a chromosome conformation capture (3C) assay, that this enhancer is capable of physically interacting with the DHRS4-AS1 promoter through chromosomal looping. The enhancer produced an eRNA, termed AS1eRNA, that enhanced DHRS4-AS1 transcription by mediating the spatial interactions of the enhancer and DHRS4-AS1 promoter in cooperation with RNA polymerase II and p300/CBP. Moreover, the distributions of activating acetyl-H3 and H3K4me3 modifications were found to be greater at the DHRS4-AS1 promoter than at the homologous duplicated regions. We propose that AS1eRNA-driven DNA looping and activating histone modifications promote the expression of DHRS4-AS1 to economically control the DHRS4 gene cluster.

The promotion of enhanced well-being among children and collaboration among families, schools, and communities is paramount and is a pressing concern in the global education sector. This necessitates that preschool teachers possess the necessary competencies for effective family-preschool partnerships (FPPs). This study explored the competencies necessary for Chinese kindergarten teachers to engage in FPP using behavioral event interviews with 30 participants. Thematic analysis identified key competency traits, and independent samples t-tests with Bonferroni correction compared collaboration competencies between outstanding and typical teachers, as well as across different career stages. Consequently, a comprehensive crisscrossing competency framework consisting of four quadrants was developed. This framework distinguishes between high-performance and general traits, as well as between stable and variable traits that may evolve across career stages. High-performance traits such as communication, expression, and relationship management should be prioritized in the training and recruitment of early childhood educators involved in FPP. In contrast, intrinsic qualities that foster successful FPP, such as child orientation, should be cultivated early and sustained throughout a teacher’s career. From a developmental perspective, this framework provides a crucial foundation for evaluating and training kindergarten teachers in the competencies essential for fostering effective FPP.

Purpose Papillary thyroid cancer (PTC), the most prevalent thyroid malignancy, is witnessing a global surge in incidence. The potassium voltage-gated channel subfamily Q member 3 (KCNQ3) is aberrantly overexpressed in PTC, yet its mechanistic contribution to oncogenesis remains unclear. Thus, we aimed to elucidate the oncogenic mechanism of KCNQ3 in PTC. Methods We integrated gene expression profiling interactive analysis (GEPIA), immunohistochemistry, and western blotting to assess KCNQ3 expression during PTC tumorigenesis and progression, and validated in vitro and in vivo using BALB/c nude mice. The functional roles of KCNQ3 were evaluated using wound-healing, transwell, and colony formation assays. Protein interactions were elucidated through co-immunoprecipitation, mass spectrometry (MS), and immunofluorescence, while estradiol (E 2 )-mediated KCNQ3 regulation was examined using chromatin immunoprecipitation–qPCR (ChIP–qPCR). The therapeutic potential of the KCNQ channel inhibitor, XE991, was also investigated. Results KCNQ3 was upregulated in PTC and drove tumor cell proliferation and migration. Mechanistically, KCNQ3 interacted with GRB2-associated regulator of MAPK1 subtype 1(GAREM1), growth factor receptor-bound protein 2(GRB2), and SOS Ras/Rac guanine nucleotide exchange factor 1 (SOS1), activating the RAS/RAF/MAPK signaling cascade to promote oncogenesis. ChIP–qPCR revealed that E 2 enhanced KCNQ3 transcription by binding estrogen receptor alpha (ESR1) to the KCNQ3 promoter. Notably, XE991 inhibited PTC cell proliferation and migration. Conclusion Our research uncovers a novel KCNQ3-driven oncogenic axis in PTC, establishing KCNQ3 as a promising therapeutic target. Our findings also establish E 2 as a KCNQ3 regulator in PTC, elucidating a mechanism underlying the female gender bias of the disease. Additionally, XE991 shows potential in PTC treatment.

The human genome, like other mammalian genomes, encodes numerous natural antisense transcripts (NATs) that have been classified into head-to-head, tail-to-tail, or fully overlapped categories in reference to their sense transcripts. Evidence for NAT-mediated epigenetic silencing of sense transcription remains scanty. The DHRS4 gene encodes a metabolic enzyme and forms a gene cluster with its two immediately downstream homologous genes, DHRS4L2 and DHRS4L1 , generated by gene duplication. We identified a head-to-head NAT of DHRS4 , designated AS1DHRS4, which markedly regulates the expression of these three genes in the DHRS4 gene cluster. By pairing with ongoing sense transcripts, AS1DHRS4 not only mediates deacetylation of histone H3 and demethylation of H3K4 in cis for the DHRS4 gene, but also interacts physically in trans with the epigenetic modifiers H3K9- and H3K27-specific histone methyltransferases G9a and EZH2, targeting the promoters of the downstream DHRS4L2 and DHRS4L1 genes to induce local repressive H3K9me2 and H3K27me3 histone modifications. Furthermore, AS1DHRS4 induces DNA methylation in the promoter regions of DHRS4L2 by recruiting DNA methyltransferases. This study demonstrates that AS1DHRS4, as a long noncoding RNA, simultaneously controls the chromatin state of each gene within the DHRS4 gene cluster in a discriminative manner. This finding provides an example of transcriptional control over the multiple and highly homologous genes in a tight gene cluster, and may help explain the role of antisense RNAs in the regulation of duplicated genes as the result of genomic evolution.

Pleckstrin homology-like domain, family A, member 1 (PHLDA1) has been reported to be expressed in many mammalian tissues and cells. However, the functions and exact mechanisms of PHLDA1 remain unclear. In this study, we found that PHLDA1 expression was significantly altered in macrophages after exposure to lipopolysaccharide (LPS) in vitro , suggesting that PHLDA1 may be involved in the regulation of TLR4 signaling pathway activated by LPS. PHLDA1 attenuated the production of LPS-stimulated proinflammatory cytokines (TNF-α, IL-6, and IL-1β). Further research showed that the phosphorylation levels of some important signal molecules in TLR4/MyD88-mediated MAPK and NF-κB signaling pathways were reduced by PHLDA1, which in turn impaired the transcription factors NF-κB and AP1 nuclear translocation and their responsive element activities. Furthermore, we found that PHLDA1 repressed LPS-induced proinflammatory cytokine production via binding to Tollip which restrained TLR4 signaling pathway. A mouse model of endotoxemia was established to confirm the above similar results. In brief, our findings demonstrate that PHLDA1 is a negative regulator of LPS-induced proinflammatory cytokine production by Tollip, suggesting that PHLDA1 plays an anti-inflammatory role through inhibiting the TLR4/MyD88 signaling pathway with the help of Tollip. PHLDA1 may be a novel therapeutic target in treating endotoxemia.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive cancer whose underlying molecular mechanisms are poorly understood. The natural antisense transcript (NAT) WRAP53 regulates p53 expression and WRAP53 protein is a component of telomerase. NATs play key roles in carcinogenesis, and although WRAP53 is known to increase cancer cell survival, its role in ESCC clinicopathology is unknown. The aim of this study was to investigate WRAP53 expression in ESCC and to correlate it with clinicopathological characteristics. WRAP53 mRNA and protein expression was measured by quantitative PCR (qRT-PCR) and western blotting, respectively, in 4 ESSC cells lines and in 45 paired ESCC and non-neoplastic esophageal mucosa tissues. To correlate WRAP53 protein expression with clinicopathological characteristics, immunohistochemistry (IHC) was performed on 134 ESCC and 85 non-neoplastic esophageal mucosa tissues. Expression of WRAP53 was detected in all ESCC cell lines and was upregulated in the ESCC tissues compared with the corresponding non-neoplastic tissues (P<0.01). More cells expressed WRAP53 protein in the ESCC tissues than in the non-neoplastic tissues (P<0.01). Overexpression of WRAP53 was significantly correlated with tumor infiltration depth (P = 0.000), clinical stage (P = 0.001), and lymph node metastasis (P = 0.025). Wrap53 expression was not correlated with age, gender, or tumor differentiation. This report indicates increased expression of WRAP53 in ESCC and that WRAP53 overexpression is correlated with tumor progression. WRAP53 may play a significant role in ESCC; accordingly, WRAP53 could be a useful biomarker for ESCC.

Background High expression of secreted matricellular protein cysteine-rich 61 ( CYR61 ) correlates with poor prognosis in colorectal cancer (CRC). Aberrant enhancer activation has been shown to correlate with expression of key genes involved in cancer progression. However, such mechanisms in CYR61 transcription regulation remain unexplored. Methods Expression of CYR61 was determined by immunohistochemistry (IHC), quantitative real-time PCR (qRT-PCR) and western blotting (WB) in CRC patients paraffin specimens and colon cell lines. ChIP-seq data of enhancer-characteristic histone modifications, in CRC tissues from the Gene Expression Omnibus (GEO) database, were reanalyzed to search for putative enhancers of CYR61 . Dual-luciferase reporter assay was used to detected enhancer activity. Physical interactions between putative enhancers and CYR61 promoter were detected by chromosome conformation capture (3C) assay. Histone modification and transcription factors (TFs) enrichment were detected by ChIP-qPCR. Additionally, biological function of enhancers was investigated by transwell migration assays. Results CRC tissues and cell lines expressed higher level of CYR61 than normal colon mucosa. Three putative enhancers located downstream of CYR61 were found in CRC tissues by ChIP-seq data reanalysis. Consistent with the ChIP-seq analysis results in the GEO database, the normal colon mucosal epithelial cell line NCM460 possessed no active CYR61 enhancers, whereas colon cancer cells exhibited different patterns of active CYR61 enhancers. HCT116 cells had an active Enhancer3, whereas RKO cells had both Enhancer1 and Enhancer3 active. Pioneer factor FOXA1 promoted CYR61 expression by recruiting CBP histone acetyltransferase binding and increasing promoter-enhancer looping frequencies and enhancer activity. CBP knockdown attenuated H3K27ac enrichment, promoter-enhancer looping frequencies, and enhancer activity. Small molecule compound 12-O-tetradecanoyl phorbol-13-acetate (TPA) treatment, which stimulated CYR61 expression, and verteporfin (VP) treatment, which inhibited CYR61 expression, confirmed that the enhancers regulated CYR61 expression. Knockdown and ectopic expression of CYR61 rescued cell migration changes induced by over-expressing and knockdown of FOXA1, respectively. Conclusions CYR61 enhancer activation, mediated by FOXA1 and CBP, occurs during CRC progression to up-regulate CYR61 expression and promote cell migration in CRC, suggesting inhibition of recruitment of FOXA1 and/or CBP to CYR61 enhancers may have therapeutic implications.