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IGF2BP3 Regulates Expression and Alternative Splicing of Genes associated with the Progression of Gastric Cancer in AGS cells

ABSTRACT: IGF2BP3 Regulates Expression and Alternative Splicing of Genes associated with the Progression of Gastric Cancer in AGS cells

PROVIDER: PRJNA1159745 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30633144_1.fastq.gz	Fastqsanger.gz
	SRR30633144_2.fastq.gz	Fastqsanger.gz
	SRR30633145_1.fastq.gz	Fastqsanger.gz
	SRR30633145_2.fastq.gz	Fastqsanger.gz
	SRR30633146_1.fastq.gz	Fastqsanger.gz

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IGF2BP3 Regulates Expression and Alternative Splicing of Genes associated with the Progression of Gastric Cancer in AGS cells

Project description:Gastric cancer has become the fifth largest malignant tumor in the world, with a mortality rate ranking fourth. IGF2BP3, as a multifunctional RNA binding protein, is involved in regulating alternative splicing and m6A modification. Research has shown that IGF2BP3 plays a carcinogenic role in the development of gastric tumors. However, there is currently relatively little research on the impact of IGF2BP3 as an RNA binding protein (RBP) on alternative splicing in gastric cancer cells. The specific function of IGF2BP3 as an RBP and its molecular mechanisms involved in the development and progression of gastric cancer are still unclear. The aim of this study is to explore the mechanism by which IGF2BP3 affects gene expression and alternative splicing by binding to mRNA, and thus plays a role in the development of gastric cancer cells. We overexpressed IGF2BP3 in gastric cancer cells (AGS) and obtained transcriptome data (RNA seq) on the effects of IGF2BP3 using high-throughput transcriptome sequencing. We then analyzed potential targets in AGS cells where transcription and alternative splicing levels are regulated by IGF2BP3, and explored the molecular mechanisms by which IGF2BP3 affects gene expression and alternative splicing in AGS cells.

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IGF2BP3 may contributes to lung tumorigenesis by regulating the alternative splicing of PKM [RIP-seq]

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IGF2BP3 may contributes to lung tumorigenesis by regulating the alternative splicing of PKM [RNA-seq]

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human gastric cancer cell AGS shTOPK LC-MSMS

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Project description:27 sample pairs were conducted exon microarrays and 25 sample pairs were retain for our further alternative splicing analysis. 260 genes showed differential expression in more than 50% of our samples and 21 genes among them were validated by real-time PCR. Six genes with splicing events, which were firstly found in gastric cancer, were confirmed by RT-PCR. Keywords: Transcriptome analysis

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Project description:Except for a few genes known to have oncogenic spliceforms in gastric cancer, the full scope of aberrant splicing in gastric oncogenesis remains unclear. In this study, we elucidated the alternative splicing events associated with gastric carcinogenesis and identified upstream regulators governing these events. We performed RNA-seq on 19 matched tumor/normal pairs and a panel of gastric cancer cell lines, and identified 361 tumor associated (TA) alternative splicing events (ASEs), which included known oncogenic ASEs in genes such as INSR, FGFR2, CD44 and KRAS. We further identified 8 splicing factors dysregulated in gastric tumors, the expression of which are correlated to the splice ratio of the TA ASEs. We thereby constructed a dysregulated splicing network in gastric cancer, consisting of alternative splicing changes correlated to their potential regulators. This network featured three potential regulatory modules centered around the splicing factors ESRP2, MBNL1 and PTPB1. Knockdown of each splicing factor led to the expected changes in splicing of approximately half of the ASEs assayed. Thus, dysregulation of the splicing factors indeed was the cause of many of the TA ASEs. Pathway enrichment analysis showed that genes affected by tumor associated splicing were pre-dominantly involved in cytoskeletal organization. Concordant with this, knockdown of the splicing factors regulating the TA ASEs led to the expected changes in trans-well migration activity. Thus, we have established for the first time a comprehensive splicing network that likely drives gastric tumor progression, based on which novel therapeutic targets can be identified for further evaluation.

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