Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 6 de 6
Mais filtros

Base de dados
Assunto principal
Intervalo de ano de publicação
Int J Environ Health Res ; : 1-13, 2021 Jun 09.
Artigo em Inglês | MEDLINE | ID: mdl-34102927


Exposure to airborne particulate matter (PM2.5) is associated with cardiovascular diseases. In order to investigate the molecular mechanisms of air pollution-induced CVDs toxicity, human umbilical vein endothelial cells (HUVECs) were exposed to PM2.5 collected from January, 2016 winter in Beijing, China. We performed RNA sequencing to elucidate key molecular mechanism of PM 2.5-mediated toxicity in HUVECs. A total of 1753 genes, 864 up-regulated and 889 down-regulated, were observed to be differentially expressed genes (DEGs). Among these, genes involved in metabolic response, oxidative stress, inflammatory response, and vascular dysfunction were significantly differentially expressed (log2 FC > 4). The results were validated by quantitative real-time PCR (qPCR) and Western blot for CYP1B1, HMOX1, IL8, and GJA4. Pathway analysis revealed that DEGs were involved in the biological processes related to metabolism, inflammation, and host defense against environmental insults. This research is providing a further understanding of the mechanisms underlying PM2.5-induced cardiovascular diseases (CVDs).

Artigo em Inglês | MEDLINE | ID: mdl-32640694


Epidemiological studies have corroborated that respiratory diseases, including lung cancer, are related to fine particulate matter (<2.5 µm) (PM2.5) exposure. The toxic responses of PM2.5 are greatly influenced by the source of PM2.5. However, the effects of PM2.5 from Beijing on bronchial genotoxicity are scarce. In the present study, PM2.5 from Beijing was sampled and applied in vitro to investigate its genotoxicity and the mechanisms behind it. Human bronchial epithelial cells 16HBE were used as a model for exposure. Low (67.5 µg/mL), medium (116.9 µg/mL), and high (202.5 µg/mL) doses of PM2.5 were used for cell exposure. After PM2.5 exposure, cell viability, oxidative stress markers, DNA (deoxyribonucleic acid) strand breaks, 8-OH-dG levels, micronuclei formation, and DNA repair gene expression were measured. The results showed that PM2.5 significantly induced cytotoxicity in 16HBE. Moreover, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and cellular heme oxygenase (HO-1) were increased, and the level of glutathione (GSH) was decreased, which represented the occurrence of severe oxidative stress in 16HBE. The micronucleus rate was elevated, and DNA damage occurred as indicators of the comet assay, γ-H2AX and 8-OH-dG, were markedly enhanced by PM2.5, accompanied by the influence of 8-oxoguanine DNA glycosylase (OGG1), X-ray repair cross-complementing gene 1 (XRCC1), and poly (ADP-ribose) polymerase-1 (PARP1) expression. These results support the significant role of PM2.5 genotoxicity in 16HBE cells, which may occur through the combined effect on oxidative stress and the influence of DNA repair genes.

Dano ao DNA , Pequim , China , Células Epiteliais , Humanos , Estresse Oxidativo , Material Particulado , Espécies Reativas de Oxigênio , Proteína 1 Complementadora Cruzada de Reparo de Raio-X
J Med Virol ; 2020 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-31916268


Human papillomavirus (HPV) infection was associated with some carcinomas, especially malignant tumors in upper digestive tract, upper respiratory tract, and genitourinary system. The mechanism of the viral transformation of normal cells is still not very clear. To investigate the tumorigenesis of epithelial cells, E6/E7-induced malignant transformation model cells were used for expression profiling analysis by performing RNA expression microarray detection. Bioinformatics analysis was applied to investigate the cellular process changes along with the E6/E7 expression in SHEE cells. The differentially expressed genes were further grouped and uploaded for Search Tool for the Retrieval of Interacting Genes analysis. The protein-protein interaction results were visualized. The hub genes and their first-neighbors genes were selected, followed by gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. The obtained results demonstrated that tumor-related biological processes began to emerge during the carcinogenesis process from 48th passage to 76th passage of SHEE cells after E6/E7 expression. Ten hub genes were identified and analyzed during the E6/E7-induced tumorigenesis. This study explores the gene expression network in the progressive transformation of immortalized esophageal epithelial cells induced by E6/E7 expression. Understanding the biological processes and hub genes that first appear during the transformation will provide some clues to the mechanism of E6/E7-induced carcinogenesis of esophageal epithelial cells.

Transl Cancer Res ; 9(3): 1818-1832, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-35117529


BACKGROUND: Esophageal cancer is one of the most common malignant tumours in humans. A series of esophageal cancer cell lines are accompanied by human papilloma virus (HPV) infection, but the mechanism behind HPV in cancer malignancy is not clear. METHODS: This research was conducted in different generations of HPV E6E7 gene-induced human foetal esophageal epithelial immortalised cells (Shantou Human Embryonic Esophageal Epithelial cell line; SHEE); the RNA sequencing transcriptomic analysis was performed to explore the mechanism of HPV infection in these cell lines. RESULTS: The results showed that there are 9,990 differential genes in late-stage cells compared with HPV18 E6E7-infected early foetal esophageal epithelial immortalised cells. Among these, 4,882 genes are upregulated, and 5,108 genes are downregulated. We used bioinformatics to analyze the expression and function of aberrantly expressed lncRNA, miRNA, mRNA and construct the competing endogenous RNA (ceRNA) network and protein protein interaction (PPI) network. CONCLUSIONS: we predicted TP53TG1 promotes to malignant transformation of SHEEs by acting as a ceRNA to competitively bind to miR-6835 and regulate IGF2 expression. We also predicted IL6 serve as prognostic biomarkers and therapy target. With these results maybe provides new insights into the mechanisms of HPV carcinogenesis in esophageal cancer.

J Cancer ; 9(22): 4242-4249, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30519325


Esophageal cancer is one of the leading malignancies globally and long non-coding RNAs (lncRNAs) have been proved to have an important role in different malignancies including esophageal cancer. However their role in disease progression is still not clear. The objective of the study was to investigate the expression and role of LINC01234 in progression of esophageal cancer cells. LncRNA LINC01234 was found to be upregulated in esophageal cancer cells by chip sequencing. The expression level of LINC01234 was detected from different esophageal cancer cell lines by qRT-PCR. After this, the LINC01234 knockdown effects on cell proliferation, migration, invasion, and apoptosis were evaluated by cell proliferation assay, wound healing assay, invasion assay, and flow cytometric analysis in vitro. Expression of lncRNA LINC01234 was found to be markedly upregulated in the CEC2 cell line. Furthermore, cell proliferation, migration and invasion were significantly (P < 0.05) suppressed as compared to negative control while apoptotic rate was also found increased as a result of the knockdown of LINC01234. Significantly upregulated expression of LINC01234 in CEC2 cells and downregulated expression after knockdown is observed. The impact of LINC01234 knockdown on cell migration, invasion, proliferation and apoptosis indicated that LINC01234 may represent a new marker and a potential therapeutic target for esophageal cancer.

Gastroenterol Res Pract ; 2018: 2028986, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29853858


Objective: The incidence of the upper gastrointestinal tumor has increased rapidly during recent decades. The relationship between local water pollution and the tumor is still not much clear, so this study was conducted to further investigate the local water pollution and its influence on the malignant cell transformation. Prevalence of human papillomavirus (HPV) in local esophageal cancer (EC) patients was also analyzed in Shenqiu County for the first time. Methods: Two-step cell transformation was used to study different sources of water in the malignant cell transformation, and the existence of 3-methylcholanthrene (3-MC) in water was analyzed from the river and shallow and deep wells. HPV DNA in tissue samples of EC patients was detected by polymerase chain reaction (PCR) and HPV diagnostic kit. Results: The river water has higher cytotoxicity than the shallow well water and induced significant cell malignant transformation, while deep well water has not shown the malignant cell transformation. In Huaihe River water, the 3-MC concentration was found higher than shallow and deep wells. An HPV infection rate was found high in patients with esophageal cancer. Conclusion: Long-term consumption of polluted water can induce malignant cell transformation, and the presence of HPV may be an important cause of cancer.