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IGF2BP1, a conserved regulator of RNA turnover in cancer [polyA RNA]

ABSTRACT: IGF2BP1, a conserved regulator of RNA turnover in cancer [polyA RNA]

PROVIDER: PRJNA675511 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13010351_1.fastq.gz	Fastqsanger.gz
	SRR13010351_2.fastq.gz	Fastqsanger.gz
	SRR13010352_1.fastq.gz	Fastqsanger.gz
	SRR13010352_2.fastq.gz	Fastqsanger.gz
	SRR13010353_1.fastq.gz	Fastqsanger.gz

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IGF2BP1, a conserved regulator of RNA turnover in cancer [polyA RNA]

Project description:The IGF2 mRNA binding protein 1 (IGF2BP1) promotes tumor progression in a multitude of solid tumors and its expression is associated with adverse prognosis. The main role proposed for IGF2BP1 in cancer cells is the stabilization of mRNAs encoding pro-oncogenic factors. Several binding studies, however, revealed a plethora of putative IGF2BP1-RNA targets. Thus, at present the main, conserved target RNAs and pathways controlled by IGF2BP1 in cancer remain elusive. In this study, we present a set of genes showing a conserved pattern of deregulation in dependence of IGF2BP1 expression in cancer-derived cell lines. By incorporating publicly available data sets, we further compiled a set of RNAs probably stabilized by IGF2BP1 in cancer and characterized them. Functional enrichment analyses revealed conserved pathways influenced by IGF2BP1 in cancer.

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IGF2BP1, a conserved regulator of RNA turnover in cancer [miRNA-seq]

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IGF2BP1 is a druggable, post-transcriptional super-enhancer of E2F-driven gene expression hallmark in cancer [IGF2BP1 KD in HepG2 (polyA RNA)]

Project description:The IGF2 mRNA-binding protein 1 (IGF2BP1) is a post-transcriptional enhancer of tumor growth. However, conserved effector pathway(s) and the feasibility of targeting IGF2BP1 in cancer cells remained elusive. We demonstrate that IGF2BP1 is a conserved regulator of E2F-driven gene expression and cancer cell cycle progression. IGF2BP1 promotes positive regulators of G1/S transition by stabilizing the respective mRNAs. This regulation is 3’UTR-, miRNA- and m6A-dependent, suggesting a conserved role of m6A-enhanced cell cycle progression across cancers. IGF2BP1 stabilizes E2F-encoding mRNAs and some of their target transcripts revealing a post-transcriptional super-enhancer role of the protein in E2F-driven gene expression. The small molecule BTYNB disrupts this super-enhancer function by impairing IGF2BP1-RNA association and consequently interferes with tumor cell proliferation and tumor growth.

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IGF2BP1 is a druggable, post-transcriptional super-enhancer of E2F-driven gene expression hallmark in cancer [IGF2BP1 KD in A549 (polyA RNA)]

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IGF2BP1, a Conserved Regulator of RNA Turnover in Cancer.

Project description:The oncofetal IGF2 mRNA-binding protein 1 (IGF2BP1) promotes tumor progression in a variety of solid tumors and its expression is associated with adverse prognosis. The main role proposed for IGF2BP1 in cancer cells is the stabilization of mRNAs encoding pro-oncogenic factors. Several IGF2BP1-RNA association studies, however, revealed a plethora of putative IGF2BP1-RNA targets. Thus, at present the main conserved target RNAs and pathways controlled by IGF2BP1 in cancer remain elusive. In this study, we present a set of genes and cancer hallmark pathways showing a conserved pattern of deregulation in dependence of IGF2BP1 expression in cancer cell lines. By the integrative analysis of these findings with publicly available cancer transcriptome and IGF2BP1-RNA association data, we compiled a set of prime candidate target mRNAs. These analyses confirm a pivotal role of IGF2BP1 in controlling cancer cell cycle progression and reveal novel cancer hallmark pathways influenced by IGF2BP1. For three novel target mRNAs identified by these studies, namely AURKA, HDLBP and YWHAZ, we confirm IGF2BP1 mRNA stabilization. In sum our findings confirm and expand previous findings on the pivotal role of IGF2BP1 in promoting oncogenic gene expression by stabilizing target mRNAs in a mainly 3'UTR, m6A-, miRNA-, and potentially AU-rich element dependent manner.

| S-EPMC8019740 | biostudies-literature

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