Tumor-associated macrophages (TAMs) and the complement system play pivotal roles in reshaping the chronic inflammatory microenvironment and driving malignant transformation. Although C1QA+ TAMs have been identified in multiple tumor types, their role in gastric cancer (GC) remains unexplored. Single-cell RNA sequencing (scRNA-seq) was performed on paired tumor tissues and adjacent tissues from three treatment-naïve patients to map macrophage heterogeneities. To evaluate the clinical and translational value of C1q, immunohistochemistry (IHC) was conducted on 100 GC samples, and C1q concentrations were measured via ELISA in plasma from a multi-center cohort of 240 patients and 100 GC tissue. Additionally, the effects of C1q-mediated THP-1-derived macrophages on the malignant behaviors of GC cells were investigated using in vitro migration. Transcriptomic analysis of 56,151 single cells successfully identified a distinct pro-inflammatory subset: C1QA+ TAMs. IHC staining demonstrated that C1q and CD163 were highly co-expressed in compromised tissues, and their elevated expression significantly correlated with poor patient prognosis. Multi-center plasma analysis revealed that elevated circulating C1q levels robustly enhanced clinical diagnostic accuracy. In vitro functional assays confirmed that C1q significantly primed M2 macrophage polarization, thereby accelerating the migration of GC cells. We first identified and functionally validated the C1QA+ TAM subset as a key driver of microenvironmental remodeling. C1q serves as a crucial mediator of macrophage polarization and holds strong promise as a novel, non-invasive biomarker for the early diagnosis.

Background:Research on human papillomavirus (HPV) vaccination willingness and behavior among patients with cervical intraepithelial neoplasia (CIN) remains limited, although such evidence is essential for improving disease prevention. Methods:A knowledge, attitude, practice (KAP) questionnaire was administered to CIN patients aged 20-60 years in Gansu Province, China to explore HPV vaccine willingness and its influencing factors. Logistic regression identified demographic factors associated with vaccination willingness, including patients >45 years. Mediation analysis tested whether knowledge indirectly influenced willingness through attitude and practice. This study also compared the differences between willingness and actual behavior, and restricted cubic splines (RCS) assessed the age-behavior relationship. Results:Among 1,012 patients, 87.45% reported willingness to receive HPV vaccination, while only 27.96% had been vaccinated. Logistic regression showed that patients who were younger, lived in urban areas, had higher education and income, reported frequent sexual activity (>4 times/month), had more sexual partners, and achieved higher KAP scores demonstrated greater willingness (all p < 0.05). Mediation analysis showed that knowledge influenced vaccination willingness mainly through attitude and practice, especially attitude (p < 0.001), while a direct effect was observed only in the chain model. Among participants >45 years old (73.96% willing), those with high-grade squamous intraepithelial lesion (HSIL) were less likely to accept vaccination. RCS revealed a significant non-linear association between age and actual vaccination behavior (p < 0.001). Conclusion:Patients showed strong willingness to vaccinate, but the actual vaccination proportion was modest. Misconceptions that infection blocks vaccination may obscure the path to protection. It is recommended to highlight the role of HPV vaccination in preventing recurrence among older HSIL patients and extend the appropriate age of vaccination.

Tumor-associated macrophages are regarded as the main driving factor for the development of malignant cancers. However, the roles of different macrophage subpopulations in gastric cancer (GC) are poorly understood. The aim of this study is to investigate the role of C1Q+ TAMs in GC.We conducted single-cell sequencing (scRNA-seq) analysis on pairs of tumor and adjacent tissues from 3 GC patients, as well as performed flow cytometry to identify of immune funtion C1Q+ TAMs. Immunohistochemistry and multiplex immunofluorescence demonstrated the relationship between C1Q+ TAMs and the poor prognosis of GC. Human plasma and tumor tissues were used to assess the value of C1q expression in the diagnosis of GC. C1QA knockdown cell lines were constructed to investigate their role in regulating macrophage polarization through fatty acid oxidation and mitochondrial respiration in vitro and in vivo. Chromatin immunoprecipitation was used to verify the mechanism by which C1Q+ TAMs regulate the expression of immunosuppressive factors through fatty acid binding protein 5 (FABP5). In vivo experiments verified the function of C1Q+ TAMs in the progression of GC.Single-cell transcriptome analysis revealed that C1Q+ TAMs highly express immunosuppressive molecules, and their high infiltration is associated with poor prognosis of GC. We collected serum samples from GC and proved that the elevated serum level of C1q has a high diagnostic accuracy. Mechanistically, C1Q+ TAMs enhance FABP5-dependent mitochondrial respiratory capacity, activating peroxisome proliferator-activated receptor-γ (PPAR-γ) and thereby promoting the expression of inhibitory molecules (Tim-3, SIRPα, PD-1, and PD-L1). Combined treatment targeting C1Q+ TAMs and using FABP5 inhibitors significantly inhibited tumor growth .GC is characterized by C1Q+ TAMs-driven an immunosuppressive microenvironment. C1q is a promising biomarker for predicting prognosis and diagnosing GC. C1q enhances the mitochondrial respiratory capacity of macrophages, thereby maintaining the tumor-promoting function. Therefore, targeting C1Q+ TAMs significantly reduces immunosuppression and enhances therapeutic efficacy.

Introduction: Methyl-N'-nitro-N-nitrosoguanidine (MNNG) is an environmental carcinogen that induces Gastric Cancer (GC). N7-methylguanosine (m7G) is a prevalent RNA modification closely linked to cancer onset and progression. However, the role of m7G in regulating gene expression during MNNG-induced gastric carcinogenesis remains unclear. This study aims to investigate the role of m7G modification in MNNG-induced GC and to identify potential downstream regulatory genes. Methods: Cell proliferation and migration were evaluated using CCK-8 and scratch assays in Malignant transformed cells (MC) and GC cells with different METTL1 expression levels. The m7G MeRIP-seq and whole-transcriptome sequencing were integrated to screen potential genes regulated by m7G modification in MC-30 cells. GO and KEGG analyses were performed for gene function. Candidate gene expression was screened and validated in MC and GC cells by RT-qPCR. Finally, we validated SLC2A3 by analyzing gene expression using the TCGA STAD cohort and 24 pairs of clinical GC samples. Results: METTL1 knockdown significantly inhibited proliferation and migration by about 25% (p < 0.001). Sequencing analysis identified SLC2A3 as a key METTL1 downstream target, with significantly altered m7G modification levels (fold change > 2, p < 0.05) and enrichment in cancer-related pathways. Clinically, SLC2A3 expression was significantly up-regulated in GC tissues versus normal controls (FC = 2.52, p < 0.001) and was significantly associated with tumor stage and prognosis in GC patients (p < 0.05). Conclusion: Our study revealed that m7G methyltransferase METTL1 plays an oncogenic role in MNNG-induced gastric carcinogenesis. SLC2A3 is a key downstream target of METTL1, which is associated with clinical progression in GC patients. These findings may provide evidence for developing prognostic biomarkers for GC.

Background The tumor microenvironment (TME) significantly impacts cancer progression and overall patient survival. However, the complexity of tumor cell-TME interactions in gastric cancer (GC) and their underlying molecular basis remain to be systematically elucidated. Methods We performed single-cell RNA sequencing (scRNA-seq) on paired tumor and adjacent tissues from 3 treatment-naïve GC patients. We conducted an in-depth characterization of the cellular composition and molecular features of the GC TME, with a particular focus on tumor-associated macrophages (TAMs) subsets and their mediated intercellular communication. Investigating the effect of C1q on the polarisation of THP-1 induced macrophages through migration and invasion experiments Results Transcriptomic analysis of 56,151 single cells identified a key TAM subset – C1QA□ TAMs. This subset is characterized by high expression of genes including C1QA, C1QB, C1QC and FN1, exhibiting a distinct M2-like macrophage phenotype. We developed a LASSO-based predictive model, C1Q-LASSO, to accurately stratify patients based on survival outcomes and chemotherapy responses, independently of established prognostic parameters. In vitro functional experiments further confirmed that C1q directly promotes malignant phenotypes in GC cells. Additionally, C1q significantly enhances the malignant progression of gastric cancer induced by M2 macrophages. Conclusions Utilizing scRNA-seq technology, this study systematically delineated the heterogeneous landscape of the GC immune microenvironment and its complex cellular interaction network at single-cell resolution. We first identified and functionally validated the C1QA□ TAM subset, demonstrating its association with poor prognosis and pro-tumorigenic functions. ### Competing Interest Statement The authors have declared no competing interest.

Low-molecular-weight polycyclic aromatic hydrocarbons (LMW-PAHs), such as the 400 μM mixture of phenanthrene and fluorene used in this study, are prevalent environmental pollutants. Induction of epithelial–mesenchymal transition (EMT) by LMW-PAHs promote cell invasion and migration and contribute to disease pathogenesis. Long non-coding RNAs (lncRNAs) regulate gene expression by acting as competing endogenous RNAs (ceRNAs) that sequester microRNAs (miRNAs), a mechanism important for modulating EMT. Previously, regulation of the PI3K/AKT pathway and EMT in A549 cells are shown to occur through the hsa_circ_0039929/miR-15b-3p_R-1/FGF2 axis. Here, the functional role of the related LINC01376/miR-15b-3p_R-1/FGF2 axis in LMW-PAH-induced EMT was examined in A549 and H1299 cells. The miR-15b-3p_R-1 was downregulated, whereas LINC01376 and FGF2 were upregulated following LMW-PAH exposure. LINC01376 overexpression enhanced EMT, migration, and invasion. Interactions between miR-15b-3p_R-1 and FGF2, as well as direct binding of LINC01376 to miR-15b-3p_R-1, were confirmed experimentally. The results indicate that, in LMW-PAH-treated cells, LINC01376 functions as a ceRNA to sponge miR-15b-3p_R-1, thereby elevating FGF2 expression and promoting EMT, migration, and invasion. Identification of the LINC01376/miR-15b-3p_R-1/FGF2 regulatory axis highlighted as a key mechanism in LMW-PAH-driven EMT and suggests its potential as a therapeutic target in PAH-related pathologies.

Objective The objective of this study is to elucidate the breast cancer (BC)-associated ceRNA regulatory network by examining the expression profiles of lncRNAs, miRNAs, and mRNAs. Methods Using RNA sequencing data from The Cancer Genome Atlas (TCGA), we compared the expression profiles of lncRNAs, miRNAs, and mRNAs between 976 breast cancer (BC) tissues and 104 matched non-cancerous samples. Then, we constructed a BRCA-specific ceRNA network and evaluated the lncRNA-miRNA-mRNA regulatory relationships. The DAVID tool was used to investigate the functional enrichment of the key, significantly dysregulated mRNAs within the ceRNA network. Moreover, we analyzed the associations between the expression levels of key genes in the ceRNA network and the clinicopathological features as well as the overall survival of the BC patients from the TCGA database. Finally, to validate our bioinformatics findings, we utilized datasets from the Gene Expression Omnibus (GEO) database (GSE42568 and GSE65194) and additionally collected 20 tissue samples from BC patients for experimental assessment. Results A total of 231 dysregulated lncRNAs, 50 miRNAs, and 1136 mRNAs were identified in BC samples from the TCGA database. Among these, 52 lncRNAs, 24 miRNAs, and 126 mRNAs were found to potentially interact through ceRNA regulatory mechanisms. Based on these key genes, we analyzed the associations between their expression levels and the clinicopathological characteristics as well as the overall survival of BC patients from TCGA. The expression of 40 lncRNAs and 20 miRNAs was significantly associated with the patients’ clinical features (P < 0.05). Notably, 12 genes (including 4 lncRNAs, 2 miRNAs, and 6 mRNAs) in the ceRNA network were statistically significantly associated with overall survival time (log-rank test, P < 0.05). Comparative analysis of the GSE42568 and GSE65194 datasets and experimental validation by RT-qPCR revealed that the expression levels and changing trends of the key genes in the ceRNA network were highly consistent with the TCGA results, confirming the reliability of our bioinformatics analysis. Conclusion This study identified key BC-related ceRNA network 52 lncRNAs, 24 miRNAs and 126 mRNAs. These key genes are worthy to further explore as potential novel biomarkers for diagnosis, classification, and prognosis of BC.

Fast-evolving nanotechnologies have supported traditional wood industries to breach the barriers and slip into tailor-made functional nanomaterials that cater to the high-tech and low-carbon era. Here, wood cell walls are in situ nanofibrillated via reversible hemicellulose supermolecular regulation toward versatile mesoporous wood nano-aerogels. The as-prepared wood nano-aerogels are composed of highly combinative high-aspect-ratio fibrils resembling native-state "core (cellulose)-shell (hemicellulose)" nanostructure, which is unreachable for conventional in situ nanofibrillation strategies involving depolymerization of non-cellulosic phases and topochemical engineering of cellulosic phase. The hemicellulose-induced in situ nanofibrillation mechanism is systematically elucidated via theoretical and experimental analysis: the enhanced swelling of hemicellulose supermolecules in specific polar cosolvent (e.g., ionic liquid/water) significantly weakens the fibril-fibril interactions within wood fiber cells without affecting the macromolecular structures. The desired structural features of in situ nanofibrillated fiber cells including high mesoporosity and microstructural homogeneity contribute to significant poroelastic dissipation and efficient stress transfer under external stress, which in turn leads to an exceptional combination of compressive strength and resilience for the as-prepared wood nano-aerogel. Furthermore, the highly hydrophilic hemicellulose "shells" of constituent nanofibrils within mesoporous cell walls endow the strong and resilient wood nano-aerogel with superior humidity responsiveness, thereby opening up vast possibilities for applications in sensing, process monitoring, and energy management systems. This work provides a feasible and environmentally benign wood nanostructure-engineered strategy for top-down manufacturing of high-performance lignocellulosic nanomaterials by leveraging the inherent functionality of wood structural constituents.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants recognized for their toxicological significance. Increasing evidence suggests that chronic exposure to low-molecular-weight PAHs (LMW-PAHs) contributes to heightened disease vulnerability and immune dysregulation, particularly among rural female populations. Recent studies have further linked a significant association between PAH exposure and gut microbiome (GM) modifications. Considering the common embryonic origin of the intestinal and respiratory systems, cross-organ communication under conditions of PAH exposure warrants deeper exploration. Although current gut–lung axis research largely emphasizes microbial metabolites such as short-chain fatty acids and bile acids, the contribution of arachidonic acid (AA) metabolites in LMW-PAH-induced pulmonary inflammation via this axis remains poorly defined. To address this knowledge gap, we developed an animal model employing integrated 16S rRNA sequencing and metabolomics approaches to systematically examine phenanthrene (Phe) and fluorene (Flu) induced GM compositional shifts and associated metabolic reprogramming. Through comprehensive profiling, we identified candidate microorganisms and metabolites potentially involved in dysbiosis-mediated pulmonary inflammation, thereby elucidating the mechanistic basis of Phe and Flu-associated health risks.

Cadmium (Cd) is a major environmental pollutant associated with male reproductive health. Lycium barbarum polysaccharides (LBP) and selenium (Se) have been shown to protect against testicular damage. Male rats (180–200 g) were selected to construct a Cd-exposed model by intraperitoneal injection with concentrations of 0.0, 0.5, 1.0, 1.5, and 2.0 mg/kg. Then, LBP and sodium selenite (Na2SeO3) were given by gavage for treatment. The results showed that Cd accumulates in the testis in a dose-dependent manner, and compared with the control group, after Cd-exposed, the testis suffered significant toxic damage. The differences in mRNA enrichment analysis between the Cd-exposed and the control groups showed that the differential genes were mainly involved in peroxidase activity, iron regulation, and cellular energy metabolism. Compared with the Cd-exposed group, LBP and Na2SeO3 intervention could antagonize the toxic damaging effects caused by Cd, and the combined intervention of LBP and Na2SeO3 could better antagonize the toxic damaging effects caused by Cd compared with the intervention alone. In general, Cd exposure caused testicular damage, increased testicular hormonal disorders, oxidative stress damage, energy metabolism disorders, and iron atrophy in the testis, while treatment with LBP and selenium alleviated the effects of Cd-induced testicular toxicity damage.

Background Reprogramming of glutamine metabolism in Gastric Cancer (GC) can significantly affect the tumor immune microenvironment and immunotherapy. This study examines the role of glutamine metabolism in the microenvironment and prognosis of gastric cancer.Methods We obtained gene expression data and clinical information of patients from the TCGA database. The patients were divided into two metabolic subtypes based on consistent clustering. A prognostic risk model containing three glutamine metabolism-related genes (GMRGs) was developed using Lasso-Cox. It was validated by the GEO validation cohort. Additionally, the immune microenvironment composition of the high- and low-risk groups was assessed using ESTIMATE, CIBERSORT, and ssGSEA. Drug sensitivity analysis was conducted using the "oncoPredict" R package.Results We outlined the distinct clinical characteristics of two subtypes and developed a prognostic risk model. The high-risk group has a poorer prognosis due to an increased expression of immune checkpoints and immunosuppressive cellular infiltration. Our analysis, which included Cox risk regression, ROC curves, and nomogram, demonstrated that this risk model is an independent prognostic factor. The TIDE score was higher in the high-risk group than in the low-risk group. Additionally, the high-risk group did not respond well to chemotherapeutic drug treatment.Conclusion This study shows that modelling glutamine metabolism is a good predictor of prognosis and immunotherapy efficacy in gastric cancer. Thus, we can better understand the role of glutamine metabolism in the development of cancer and use these insights to develop more targeted and effective treatments.

Objective The medical treatment of cancer patients has caused a huge burden on the financial expenditure of the government, so it is crucial to evaluate whether the financial expenditure of public medical care. The aim of this study was to identify risk populations of esophageal cancer (EC) in Liangzhou through epidemiological data and evaluate the feasibility and cost-effectiveness of early screening in these populations. Methods We collected data on EC incidence and follow-up from 2009 to 2021 in the regions of Liangzhou and Jingtai in Gansu Province. We used spatial analysis and regional investigation the incidence data of EC reporting area to analyze the prevalence of EC within Liangzhou and Jingtai, the impact of lifestyle, heavy metals and nitrosamines on EC. Subsequently, we conducted a health economics assessment based on the Chinese government's regional investment in EC screening in Gansu Province in the past five years, with a view to optimizing cancer prevention measures in areas with high incidence of EC. Results From 2009 to 2021, the incidence of EC in Liangzhou remained high with an average annual incidence of 45.23 per100,000, there were 8 communities and townships with the incidence of EC higher than 70/100,000 in Liangzhou. Drinking alcohol, intake of red meat, salted food, dried food, fried food and dry thinness were risk factors for EC. The trace elements ( iron, copper and zinc) and NMEA, NDEA and NDPA in drinking water of Liangzhou were higher than those in Jingtai County, suggested that the residents of Liangzhou District are exposed to higher environmental carcinogenic risk. In the systematic health economics evaluation of the EC screening, we found that the screening cost amounted to 1,1407200 yuan, and the benefit totaled 1,9763200 yuan, resulting in a cost-benefit ratio (CBR) of 1:1.73. Conclusions This study identified high-incidence areas and key populations of EC. This approach guided the implementation of targeted EC screening in specific area, proving to be a cost-effective and efficient screening method. The adoption of this approach should be widely applied in the prevention and control of EC in the future, and provides an important basis for the clinical benefit and early screening of patients with EC.

BackgroundGastric carcinogenesis is a multifactorial and complex process, in which long non-coding RNAs (lncRNAs) play important roles as oncogenes or antioncogenes. Research has found that the expression of lncRNA LINC02859 is down-regulated in gastric cancer tissues and correlated with the degree of tumor differentiation and TNM stage, and also plays an important role in the development of malignant transformation of cells induced by environmental carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but its mechanism of action is still unclear. ObjectiveTo explore the role and potential regulatory mechanism of gastric cancer-associated lncRNA LINC02859 in MNNG-induced malignant transformation of human normal gastric mucosal cells (GES-1). MethodsA total of 110 gastric cancer patients from a high incidence area of gastric cancer in Gansu Province were selected, and their cancer tissues and normal gastric mucosa tissues adjacent to the cancer were collected to detect the expression level of LINC02859 by real-time quantitative PCR (RT-qPCR). High-throughput sequencing and bioinformatics analysis of the tissues were used to identify the potential signaling pathways regulated by the genes co-expressed with LINC02859. GES-1 cells at 70%-80% cell fusion with low cell passage number and normal morphology were incubated with 0, 0.25 and 0.5 μmol·L−1 MNNG solution for 48 h and the LINC02859 expression level was detected. Cell proliferation activity was detected by Cell Counting Kit-8 (CCK-8), clone formation was detected by plate clone formation assay, and cell migration ability was detected by scratch assay to evaluate the effects of MNNG on cell morphology and function. The expression levels of key proteins of Wnt signaling pathway were detected by RT-qPCR and Western blotting. Results The RT-qPCR results showed that LINC02859 was lowly expressed in the gastric cancer tissues compared with the paracancerous tissues, and the difference was statistically significant (P < 0.05). The pathway enrichment analysis showed that LINC02859 potentially regulated the Wnt pathway. The in vitro malignant transformation assay suggested that after the MNNG exposure, the malignant cells of passage 5 (MC-5) had altered morphology, increased number of colony formation, and higher proliferation and migration ability than the control cells; compared with the normal GES-1 cells, LINC02859 gene expression levels were reduced in the 0.25 μmol·L−1 and the 0.5 μmol·L−1 MNNG-exposed GES-1 cells; the expression levels of key proteins of the Wnt pathway, transcription factor 7 (TCF7), Axis inhibitor (Axin1), phosphorylation of glycogen synthase kinase-3 beta (p-GSK-3β), casein kinase 1 (CK1), and β-catenin, were elevated in the cells after 0.5 μmol·L−1 MNNG exposure (P < 0.05); whereas, overexpression of LINC02859 suppressed the activating effect of MNNG on the Wnt pathway. ConclusionLINC02859 is lowly expressed in the cancer tissues of gastric cancer patients. MNNG exposure induces morphological and functional changes in GES-1 cells, down-regulated expression of LINC02859, and activation of the Wnt signaling pathway; overexpression of LINC02859 inhibits the activation of the Wnt signaling pathway in the gastric carcinogenesis induced by MNNG exposure.

N-methyl-n’-nitroso-n’-nitroso guanidine (MNNG) can induce esophageal squamous cell carcinoma (ESCC), and microRNAs are associated with the development of ESCC and may serve as potential tumor prognostic markers. Thus, the aim of this study was to evaluate the potential function of miR-101-3p in MNNG-induced ESCC. An investigation of risk factors in patients with ESCC was carried out and the concentration of nine nitrosamines in urine samples was detected by the SPE-GC-MS technique. Then, we performed cancer tissue gene sequencing analysis, and RT-qPCR verified the expression level of miR-101-3p. Subsequently, the relationship between miR-101-3p potential target genes and the ESCC patients’ prognosis was predicted. Finally, we investigated the function of miR-101-3p in MNNG-induced ESCC pathogenesis and the regulatory mechanism of the signaling pathway by in vivo and in vitro experiments. The results revealed that high dietary nitrosamine levels are high-risk factors for ESCC. MiR-101-3p is down-regulated in ESCC tissues and cells, and its potential target genes are enriched in cell migration and cancer-related pathways. MiR-101-3p target genes include AXIN1, CK1, and GSK3, which are involved in the regulation of the Wnt signaling pathway. MiR-101-3p overexpression promotes apoptosis and inhibits the proliferation and migration of Eca109 cells. The Wnt pathway is activated after subchronic exposure to MNNG, and the Wnt pathway is inhibited by the overexpression of miR-101-3p in Eca109 cells. Down-regulated miR-101-3p may exert tumor suppressive effects by regulating the Wnt pathway and may be a useful biomarker for predicting ESCC progression.

As a representative item of chemical carcinogen, MNNG is closely associated with the onset of gastric cancer (GC), where N6-methyladonosine (m6A) RNA methylation is recognized as a critical epigenetic event. In our previous study, we found that the m6A modification by methyltransferase METTL3 was up-regulated in MNNG-exposed malignant GES-1 cells (MC cells) compared to control cells in vitro, and long non-coding RNA SNHG7 as a downstream target of the METTL3. However, the functional role of METTL3 in mediating the SNHG7 axis in MNNG-induced GC remains unclear. In the present study, we continuously investigate the functional role of METTL3 in mediating the SNHG7 axis in MNNG-induced GC. RIP-PCR and m6A-IP-qPCR were used to examine the molecular mechanism underlying the METTL3/m6A/SNHG7 axis in MNNG-induced GC. A METTL3 knockout mice model was constructed and exposed by MNNG. Western blot analysis, IHC analysis, and RT-qPCR were used to measure the expression of METTL3, SNHG7, and EMT markers. In this study, we demonstrated that in MNNG-induced GC tumorigenesis, the m6A modification regulator METTL3 facilitates cellular EMT and biological functions through the m6A/SNHG7 axis using in vitro and in vivo models. In conclusion, our study provides novel insights into critical epigenetic molecular events vital to MNNG-induced gastric carcinogenesis. These findings suggest the potential therapeutic targets of METTL3 for GC treatment.

By using random sampling and the questionnaire star survey method,this study investigated and analyzed the situation of 182 students who intended to change their majors during the second semester of 2020 and 2021 at a comprehensive university.The aim of the study was to understand the relevant situation of changing majors among undergraduate students in comprehensive universities and to provide suggestions and recommendations for the balanced development of majors and the optimization of policies related to changing majors.

As a representative example of an environmental chemical carcinogen, MNNG exposure is closely associated with the onset of gastric cancer (GC) where N6-methyladenosine (m6A) RNA methylation tends to be the critical epigenetic event. However, the effect of m6A modification on long non-coding RNAs (lncRNAs) in MNNG-induced GC onset is still unclear. To address the above issue, based on the Methylated RNA immunoprecipitation sequencing (MeRIP-seq) data of MNNG-induced malignant cells (MCs) and GC cells, we comprehensively analyzed the MNNG exposure-associated vital lncRNAs. MeRIP-seq analysis identified 1432 lncRNA transcripts in the MC cell, and 3520 lncRNA transcripts were found to be m6A modified in the GC cell, respectively. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that MNNG exposure could spark cellular localization change, which might be the critical cellular note variation for malignant transformation. We demonstrated that METTL3 is responsible for N6 methylation of lncRNAs and identified SNHG7 as a downstream target of METTL3. More importantly, we observed that SNHG7 was progressively up-regulated during gastric carcinogenesis by MNNG exposure. Finally, we investigated SNHG7 expression in different stages of GC malignancies and found that elevated SNHG7 expression correlated with advanced clinical features and poor prognosis in GC. In conclusion, our study found for the first time that METTL3 regulates the m6A methylation level of lncRNA SNHG7 and its expression in MNNG exposure-induced GC, suggesting that SNHG7 as a predictive biomarker or therapeutic target for GC.

目的 了解兰州某高校公共卫生相关专业新生的专业录取满意度和转专业意愿情况,为提高公共卫生学科专业思想稳定性和人才培养质量提供依据.方法 自行设计调查问卷对该校公共卫生学院2017-2021级新生专业录取满意度和转专业意愿进行调查;单因素和二元Logistic回归用于分析新生录取专业满意度和转专业意愿的影响因素,P＜0.05被认为差异有统计学意义;同时,收集该学院2017-2021级学生录取和转专业情况并进行分析.结果 2017-2021级公共卫生相关专业新生对录取专业满意、有转专业意愿的比例分别为48.60％～67.55％、47.24％～63.55％,新生最终转出率为25.98％～30.77％.进一步分析发现,性别、民族、第一志愿、对公共卫生的认知程度等因素影响新生的专业录取满意度;多因素分析发现性别、录取专业、第一志愿、录取专业满意度等是新生转专业意愿的重要影响因素.结论 公共卫生相关专业新生的专业录取满意度和专业稳定性较低,而拟转专业和最终转专业的比例较高,因此需要有一定的措施加强新生专业满意度和思想稳定性,提高公共卫生人才培养质量.

As the representative item of environmental chemical carcinogen, MNNG was closely associated with the onset of Gastric cancer (GC), while the underlying mechanisms remain largely unknown. Here, we comprehensively analyzed the potential clinical significance of METTL3 in multiple GC patient cohorts. Additionally, we demonstrated that long-term exposure to MNNG elevated METTL3 and EMT marker expression by in vitro and in vivo models. Furthermore, the depletion of METTL3 impacted the proliferation, migration, invasion, and tumorigenesis of MNNG malignant transformation cells and GC cells. By me-RIP sequencing, we identified a panel of vital miRNAs potentially regulated by METTL3 that aberrantly expressed in MNNG-induced GC cells. Mechanistically, we showed that METTL3 meditated miR-1184/TRPM2 axis by regulating the process of miRNA-118. Our results provide novel insights into critical epigenetic molecular events vital to MNNG-induced gastric carcinogenesis. These findings suggest the potential therapeutic targets of METTL3 for GC treatment.