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Transcriptome analysis of lncRNA–mRNA interactions in chronic atrophic gastritis

ABSTRACT: Transcriptome analysis of lncRNA–mRNA interactions in chronic atrophic gastritis

PROVIDER: PRJNA641806 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12088620_1.fastq.gz	Fastqsanger.gz
	SRR12088620_2.fastq.gz	Fastqsanger.gz
	SRR12088621_1.fastq.gz	Fastqsanger.gz
	SRR12088621_2.fastq.gz	Fastqsanger.gz
	SRR12088622_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of lncRNA–mRNA interactions in chronic atrophic gastritis

Project description:The aims of this study are to identify prognosis-related differentially expressed lncRNAs and mRNAs in chronic atrophic gastritis (CAG). By analysis of high-throughput whole-transcriptome sequencing data, levels of lncRNAs and mRNAs between CAG and chronic nonatrophic gastritis (CNAG) were compared pairwisely. Finally, 97,282 lncRNA transcripts and 20,307 mRNA transcripts were acquired, including 50 upregulated and 66 downregulated lncRNAs and 377 upregulated and 763 downregulated mRNAs in CAG were identified (P< 0.05, fold change ≥2). Moreover, the interactions of the differentially expressed genes in CAG were investigated by gene ontology (GO) enrichment analysis, showing that the enriched genes are involved in many biological processes, such as MAP kinase activity, heat generation, and protein modification processes. Through the construction of co-expression networks of the differentially expressed genes in CAG, three critical lncRNAs nodes were identified as potential key factors in CAG. Eight mRNAs common in both the co-expression network and the protein-protein interaction (PPI) network were selected via Venn analysis, including DGKA, EIF6, HKDC1, DHRS11, CPS1, KRT15, TESPA1, and CDHR2.Finally, the expression levels of five differentially expressed lncRNAs in CAG were confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). In conclusion, this study presents novel promising biomarkers for the diagnosis of CAG.

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Exploration of lncRNA/circRNA-miRNA-mRNA networks in patients with chronic atrophic gastritis in plateau areas [lncRNA]

Project description:Higher incidence of chronic atrophic gastritis (CAG) is generally considered a precancerous lesion of gastric cancer (GC). Therefore, the early diagnosis and treatment of CAG, especially in Tibetan Plateau areas, play an important role in the prevention of GC. The atrophic and non-atrophic gastric mucosal tissue samples from 7 patients with chronic gastritis (CG) and cancer tissue samples from 3 patients with GC were collected. High-throughput sequencing was performed to identify the differentially expressed in lncRNAs, circRNAs, miRNAs, and mRNAs, followed by the construction of competitive endogenous RNA (ceRNA) regulatory networks (lncRNA/circRNA-miRNA-mRNA network) in CAG. Those differentially expressed mRNAs with the same expression trend in both CAG and GC were further identified. Two datasets (GSE153224 and GSE163416), involving data in non-Tibetan Plateau areas, were used to further screen out plateau-specific mRNAs in CAG, followed by identification of the plateau-specific and ferroptosis related mRNAs. GO and KEGG enrichment analysis were performed to investigate the biological functions of plateau-specific mRNAs in CAG. This study may provide useful information for identifying potential biomarkers for the diagnosis of CAG.

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Expression data from biopsies with chronic atrophic gastritis and gastric cancer

Project description:Gastric cancer is an important health problem because it is difficult to diagnose and treat in advanced stage. This makes that the prognosis of gastric cancer patients remains scarce. Currently it is known that the cause of gastric cancer is attributed to chronic infection with Helicobacter pylori. Its persistent infection leads to development of chronic atrophic gastritis that is considered as a predecessor stage of intestinal-type gastric cancer. The understanding of the alteration of molecular mechanisms during the early stages of the development of gastric cancer, and the identification of their potential biomarkers can allow a rapid diagnosis that leads to an improvement diagnosis and increase the patient’s prognosis. We analyzed gene expression profiles of patients with chronic atrophic gastritis and gastric cancer through microarray analysis, functional enrichment analysis and validation of gene expression by quantitative PCR. Gene expression profiles in patients with chronic atrophic gastritis showed molecular changes of the gastric mucosa, which leads to intestinal metaplasia and subsequently, gastric cancer. In gastric cancer the gene expression profile showed the stage of tumor progression, the product of these genes are potential biomarkers of early stages of cancer that can be potential therapeutic targets. Accordingly, the transcriptome analysis revealed several gene groups are related to development of chronic atrophic gastritis, some of which were inhibited in gastric cancer patients. The increased expression of CLDN1, CLDN7, OLFM4, c-Myc and MMP-9 genes in chronic atrophic gastritis and gastric cancer point outs to their use as promising biomarkers for the early diagnosis of gastric cancer.

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Project description:Helicobacter pylori colonization of the human stomach is a strong risk factor for gastric cancer. To investigate H. pylori-induced gastric molecular alterations, we used a Mongolian gerbil model of gastric carcinogenesis. Histologic evaluation revealed varying levels of atrophic gastritis (a premalignant condition characterized by parietal and chief cell loss) in H. pylori-infected animals, and transcriptional profiling revealed a loss of markers for these cell types. We then assessed the spatial distribution and relative abundance of proteins in the gastric tissues using imaging mass spectrometry and liquid chromatography with tandem mass spectrometry (LC-MS/MS). We detected striking differences in protein content of corpus and antrum tissues. 492 proteins were preferentially localized to the corpus in uninfected animals. The abundance of 91 of these proteins was reduced in H. pylori-infected corpus tissues exhibiting atrophic gastritis compared to infected corpus tissues with non-atrophic gastritis or uninfected corpus tissues; these included numerous proteins with metabolic functions. Fifty proteins localized to the corpus in uninfected animals were diffusely delocalized throughout the stomach in infected tissues with atrophic gastritis; these included numerous proteins with roles in protein processing. Corresponding alterations were not detected in animals infected with a H. pylori ∆cagT mutant (lacking Cag type IV secretion system activity). These results indicate that H. pylori can cause loss of proteins normally localized to the gastric corpus as well as diffuse delocalization of corpus-specific proteins, resulting in marked changes in the normal gastric molecular partitioning into distinct corpus and antrum regions.

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