exosomal-linc01614-from-gastric-cancer-cells-drives-treg

Exosomal LINC01614 from Gastric Cancer Cells Drives Treg Differentiation

This study aimed to investigate the potential mechanism by which LINC01614, a long non-coding RNA (lncRNA), regulates the immune microenvironment of ...

single-cell-rna-sequencing-for-profiling-ganglionic-aganglionic

Single-cell RNA Sequencing for Profiling Ganglionic and Aganglionic Colonic Segments from Patients with Hirschsprung Disease

Hirschsprung disease (HSCR) is a congenital intestinal motility disorder characterized by the absence of enteric neurons in the distal bowel. Compared ...

The Second Affiliated Hospital of Zunyi Medical University

Endocrine-disrupting chemical (EDC) has been thought to play a role in non-alcoholic fatty liver disease (NAFLD). However, the toxic effects of Nonylphenol (NP), an EDC, on non-alcoholic fatty liver disease have never been elaborated. This study aimed to investigate whether exposure to NP could induce NAFDL, a promoting effect of high-sucrose-high-fat diet (HSHFD) on the adverse effects caused by NP was evaluated. Fourth eight male rats were assigned to four groups and each group was treated with a specific testing sample: normal-diet (ND) control group (C-ND); normal diet plus NP (180mg/kg/day) group (NP-ND); high-sucrose-high-fat-diet control group (C-HSHFD); HSHFD plus NP (180mg/kg/day) group (NP-HSHFD). At the age of 80 day, sonogram presents diffusely increased hepatic echogenicity in the NP-HSHFD group. The oblique diameter of liver in the NP-HSHFD group was significantly bigger than that in both the C-ND and NP-ND groups. At the age of 90 day, exposure to NP-HSHFD and NP-ND caused a significant increase in NP concentration in liver as compared to the C-ND group. The rats in the groups treated with NP+ND, HSHFD and NP+HSHFD produced significant increases in the body weight, fat weight and FMI, respectively, when compared to the C-ND group. The liver weight and hepatosomatic indexes (HIS) of rats in the NP-HSHFD group are higher than those in the C-HSHFD group. Exposure to NP-HSHFD induced the increases in plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL) as compared to the C-ND group. Morphological examination of liver tissue from rats exposed to NP+HSHFD shown steatosis with marked accumulation of lipid droplets, hepatocellular ballooning degeneration and inflammatory cell infiltration. Chronic exposure to NP might induce NAFLD in male rats. The high-sucrose-high-fat diet accelerates and exacerbates the development of NAFLD caused by NP exposure.

Adverse effects of chronic exposure to nonylphenol on non-alcoholic fatty liver disease in male rats.

Exposure to environmental endocrine disruptors (EEDs) contributes to the pathogenesis of many metabolic disorders. Here, we have analyzed the effect of the EED-nonylphenol (NP) on the promotion of non-alcoholic fatty liver disease (NAFLD) in rats fed high sucrose-high fat diet (HSHFD). Fifty Sprague-Dawley rats were divided into five groups: controls fed a normal diet (C-ND); HSHFD-fed controls (C-HSHFD); and rats fed a HSHFD combined with NP at doses of 0.02 μg/kg/day (NP-L-HSHFD), 0.2 μg/kg/day (NP-M-HSHFD), and 2 μg/kg/day (NP-H-HSHFD). Subchronic exposure to NP coupled with HSHFD increased daily water and food intake (p < 0.05), hepatic echogenicity and oblique liver diameter (p < 0.05), and plasma levels of alanine aminotransferase, aspartate aminotransferase, total cholesterol, triglycerides, and low density lipoprotein cholesterol (p < 0.05). Combined exposure to NP and HSHFD induced macrovesicular steatosis with dilation and congestion of the central vein, liver inflammatory cell infiltration, and expression of genes regulating lipid metabolism, SREBP-1C, FAS, and Ucp2. These results demonstrate that NP aggravates NAFLD in HSHFD-treated rats by up-regulating lipogenic genes, and that HSHFD increases the toxic effects of NP. Thus subchronic NP exposure may lead to NAFLD, especially when combined with a high-sucrose/high-fat diet.

Nonylphenol aggravates non-alcoholic fatty liver disease in high sucrose-high fat diet-treated rats.

Tumor-associated macrophages contribute to cell growth, development, and metastasis in various cancers. However, the underlying mechanisms of M2 macrophage that modulate the progression of gastric cancer (GC) remain largely unknown. In this study, we detected the ratio of macrophages in GC tissues and found that the proportion of M2 macrophages was increased in GC tissues. We then co-cultured GC cells with M1 and M2 macrophages, respectively, and then assessed cell proliferation and tumorigenicity of GC cells by MTT and colony formation assay. The results indicated that M2 macrophages promoted the proliferation of GC cells, but M1 not. Besides, GW4869, an exosomes inhibitor, reduced the effects induced by M2 macrophage. Then, we isolated and identified exosomes derived from M1 and M2 macrophage, and confirmed that the exosomes could be taken up by GC cells. We demonstrated that M2 macrophage-exosomes could induce the proliferation and tumorigenesis  and . Moreover, miR-487a was enriched in M2 macrophage-exosomes and further determined that miR-487a exert the functions by targeting TIA1. In conclusion, exosomal miR-487a derived from M2 macrophage promotes the proliferation and tumorigenesis in gastric cancer, and the novel findings might be helpful to the development of novel diagnostic and therapeutic methods in GC.

Exosomal miR-487a derived from m2 macrophage promotes the progression of gastric cancer.

Recently, the effect of endocrine-disrupting chemicals on the cancer procession has been a concern. Nonylphenol (NP) is a common environmental estrogen that has been shown to enhance the proliferation of colorectal cancer (CRC) cells in our previous studies; however, the underlying mechanism remains unclear. In this study, we confirmed the increased concentration of NP in the serum of patients with CRC. RNA sequencing was used to explore the differentially expressed genes after NP exposure. We found 16 upregulated genes and 12 downregulated genes in COLO205 cells after NP treatment. Among these differentially expressed genes, we found that coiled-coil domain containing 80 (CCDC80) was downregulated by NP treatment and was associated with CRC progression. Further experiments revealed that the overexpression of CCDC80 significantly suppressed NP-induced cell proliferation and recovered the reduced cell apoptosis. Meanwhile, the overexpression of CCDC80 significantly inhibited the activation of ERK1/2 induced by NP treatment. ERK1/2 inhibitor (PD98059) treatment also suppressed NP-induced CRC cell growth, but the overexpression of CCDC80 did not enhance the effect of ERK1/2 inhibitor. Taken together, NP treatment significantly inhibited the expression of CCDC80, and the overexpression of CCDC80 suppressed NP-induced CRC cell growth by inhibiting the activation of ERK1/2. These results suggest that NP could induce CRC cell growth by influencing the expression of multiple genes. CCDC80 and ERK1/2 inhibitors may be suitable therapeutic targets in NP-related CRC progression.

Coiled-Coil Domain Containing 80 Suppresses Nonylphenol-Induced Colorectal Cancer Cell Proliferation by Inhibiting the Activation of ERK1/2.

Nonylphenol (NP) is a widely used chemical, which has been considered a kind of endocrine-disrupting chemical and is involved in the occurrence and development of many types of cancers. Our recent studies demonstrated that NP exposure is related to colorectal cancer (CRC) progression. In this study, we also found epithelial-mesenchymal transition (EMT) promoted by NP treatment in CRC cells. However, the mechanism of NP on tumor metastasis is still unclear. In this study, we focused on the effect of the regulator of cell cycle (RGCC) induced by NP treatment. The cancer genome atlas (TCGA) analysis suggested that the expression of RGCC increased in CRC tissues, and our clinical samples showed that the expression of RGCC in tumor tissues is positively correlated with the serum level of NP in CRC patients. Further studies revealed that overexpression of RGCC could enhance the NP-induced EMT process in CRC cells and activate ERK signaling pathways. Inhibiting ERK signaling by ERK inhibitors or the knockdown of RGCC could attenuate the NP-induced EMT process. In addition, both RGCC overexpression and NP treatment could activate ERK pathways and attenuate the effect of ERK inhibitors on the EMT process in CRC cells. Altogether, this study demonstrated that NP could induce cell invasion and migration by increasing the expression of RGCC to enhance the EMT process, which might be through the activation of ERK signaling pathways. This finding supported a potential target for studying NP exposure-related colorectal cancers.

Nonylphenol Promoted Epithelial-Mesenchymal Transition in Colorectal Cancer Cells by Upregulating the Expression of Regulator of Cell Cycle.

Colorectal cancer (CRC) represents a leading cause of cancer-related deaths. Metronidazole (MNZ) is exceedingly implicated in CRC. This study explored the roles of MNZ in mouse CRC occurrence and liver metastasis (CRLM).

Effects of metronidazole on colorectal cancer occurrence and colorectal cancer liver metastases by regulating Fusobacterium nucleatum in mice.

Sleep disorders significantly impact the quality of life for many individuals, which remain largely unrecognized. It is widely believed that dietary nutrient intake plays a crucial role in promoting healthy sleep patterns. However, there is lack of research focusing on cancer survivors. This study utilized the National Health and Nutrition Examination Survey (NHANES) database to investigate the correlation between dietary nutrient intake and sleep disorders in cancer survivors. Analyzing data from 2882 cancer survivors in NHANES spanning from 2005 to 2018. Dietary nutrient intake was evaluated through two 24-h dietary recalls. Weighted multivariable logistic regression model was employed to further applied to explore the association between dietary fiber intake and sleep disorders while controlling for relevant confounding factors. Additionally, the nonlinear and dose-response relationships were explored using restricted cubic spline (RCS) regression along with smooth curve fitting and threshold effect analysis. Stratified analysis and interaction analysis were conducted to assess the consistency of the results. Univariable and multivariable analysis demonstrated that dietary fiber intake showed negative correlation with sleep disorders (P < 0.05). Treating dietary fiber intake as continuous variable. After accounting for all covariates, the study reaffirmed the protective role of dietary fiber (odds ratio [OR]: 0.99, 95% confidence interval [CI]: 0.98-0.99, P = 0.044). Analysis of dietary fiber intake in quartiles further supported this trend (P < 0.001). Interestingly, further investigations indicated that dietary fiber intake was not associated with sleep apnea, insomnia, restless legs syndrome, or other types of sleep disorders (P > 0.05). Notably, no statistically significant interactions were observed in all subgroup analyses except poverty income ratio (PIR) (P for interaction < 0.05), indicating that the protective effect of dietary fiber on sleep disorders was more pronounced in individuals with PIR ≥ 2.5. Our results suggest that adequate dietary fiber intake may be beneficial dietary strategy to reduce sleep disorders in cancer survivors.

Associations between dietary nutrient intake and sleep disorders in cancer survivors base on NHANES 2005 to 2018.

Nonylphenol (NP) is a common environmental contaminant and endocrine disruptor. Our previous research demonstrated that NP could promote the proliferation and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells; however, the specific mechanism remains unclear. miRNA sequencing revealed that NP upregulated the expression levels of microRNA(miR)-151a-3p in CRC. Analysis of The Cancer Genome Atlas (TCGA) data revealed increased expression levels of miR-151a-3p in CRC tissues. The present experiments showed that NP could activate the WNT/β-catenin signaling pathway, and promoted the migration and invasion of CRC cells by increasing the expression levels of miR-151a-3p. Through bioinformatics analysis and dual-luciferase reporter assays, Fyn-related kinase (FRK) was identified as a target gene of miR-151a-3p. Knockdown of FRK promoted NP-induced EMT in CRC cells and activated the WNT/β-catenin signaling pathway, while overexpression had the opposite effect. In summary, the present study demonstrated that NP could inhibit FRK expression via miR-151a-3p, activate the WNT/β-catenin signaling pathway, and promote EMT in CRC cells.

Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p.

Anemia is a prevalent issue among cancer survivors, which greatly affects their quality of life and overall prognosis. The Naples Prognostic Score (NPS), an inflammation-based prognostic tool, is increasingly acknowledged for its potential in predicting clinical outcomes. This study aims to assess the correlation between anemia status, prognosis, and NPS in cancer survivors.

Association of Naples Prognostic Score with anemia in cancer survivors: a study based on NHANES database.

To explore early surgical indications and clinical predictive factors for neonatal necrotizing enterocolitis (NEC) to improve the prognosis of affected infants.

ArticleTotal : 2	Year
Publication title Cited by 1	2026
Publication title	2026

Article	Year
Adverse effects of chronic exposure to nonylphenol on non-alcoholic fatty liver disease in male rats. PloS one\| PubMed ID: 28686624	2017
Nonylphenol aggravates non-alcoholic fatty liver disease in high sucrose-high fat diet-treated rats. Scientific reports\| PubMed ID: 29459774	2018
Exosomal miR-487a derived from m2 macrophage promotes the progression of gastric cancer. Cell cycle (Georgetown, Tex.)\| PubMed ID: 33522393	2021
Coiled-Coil Domain Containing 80 Suppresses Nonylphenol-Induced Colorectal Cancer Cell Proliferation by Inhibiting the Activation of ERK1/2. Frontiers in cell and developmental biology\| PubMed ID: 34746152	2021
Nonylphenol Promoted Epithelial-Mesenchymal Transition in Colorectal Cancer Cells by Upregulating the Expression of Regulator of Cell Cycle. Chemical research in toxicology\| PubMed ID: 36074022	2022
Effects of metronidazole on colorectal cancer occurrence and colorectal cancer liver metastases by regulating Fusobacterium nucleatum in mice. Immunity, inflammation and disease\| PubMed ID: 38018574	2023
Associations between dietary nutrient intake and sleep disorders in cancer survivors base on NHANES 2005 to 2018. Scientific reports\| PubMed ID: 39478148	2024
Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p. Discover oncology\| PubMed ID: 39832042	2025
Association of Naples Prognostic Score with anemia in cancer survivors: a study based on NHANES database. Frontiers in oncology\| PubMed ID: 40018412	2025
Analysis of early surgical indications and related factors in neonatal necrotizing enterocolitis. Frontiers in pediatrics\| PubMed ID: 40464051	2025

Xuefeng Yang

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