IGF2BP1, a conserved regulator of RNA turnover in cancer [miRNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA675554 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13010545.fastq.gz | Fastqsanger.gz | |||
| SRR13010546.fastq.gz | Fastqsanger.gz | |||
| SRR13010547.fastq.gz | Fastqsanger.gz | |||
| SRR13010548.fastq.gz | Fastqsanger.gz | |||
| SRR13010549.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
Similar Datasets
Project description:IGF2BP1, a conserved regulator of RNA turnover in cancer
| PRJNA675562 | ENA
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.
2021-03-22 | GSE161099 | GEO
Project description:IGF2BP1, a conserved regulator of RNA turnover in cancer [total RNA]
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Project description:IGF2BP1, a conserved regulator of RNA turnover in cancer [polyA RNA]
| PRJNA675511 | ENA
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.
2021-03-22 | GSE161087 | GEO
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.
2021-03-22 | GSE161086 | GEO
Project description:The oncofetal mRNA-binding protein IGF2BP1 and the transcriptional regulator SRF modulate gene expression in cancer. In cancer cells, we demonstrate that IGF2BP1 promotes the expression of SRF in a conserved and N6-methyladenosine (m6A) dependent manner by impairing the miRNA-directed decay of the SRF mRNA. This results in enhanced SRF-dependent transcriptional activity and promotes tumor cell growth and invasion. At the post-transcriptional level, IGF2BP1 sustains the expression of various SRF-target genes. The majority of these SRF/IGF2BP1-enhanced genes, including PDLIM7 and FOXK1, shows conserved upregulation with SRF and IGF2BP1 synthesis in cancer. PDLIM7 and FOXK1 promote tumor cell growth and were reported to enhance cell invasion. Consistently, 35 SRF/IGF2BP1-dependent genes showing conserved association with SRF and IGF2BP1 expression indicate a poor overall survival probability in ovarian, liver and lung cancer. In conclusion, these findings identify the SRF/IGF2BP1-, miRNome- and m6A-dependent control of gene expression as a conserved oncogenic driver network in cancer.
2018-10-10 | GSE116179 | GEO
Project description:The oncofetal mRNA-binding protein IGF2BP1 and the transcriptional regulator SRF modulate gene expression in cancer. In cancer cells, we demonstrate that IGF2BP1 promotes the expression of SRF in a conserved and N6-methyladenosine (m6A) dependent manner by impairing the miRNA-directed decay of the SRF mRNA. This results in enhanced SRF-dependent transcriptional activity and promotes tumor cell growth and invasion. At the post-transcriptional level, IGF2BP1 sustains the expression of various SRF-target genes. The majority of these SRF/IGF2BP1-enhanced genes, including PDLIM7 and FOXK1, shows conserved upregulation with SRF and IGF2BP1 synthesis in cancer. PDLIM7 and FOXK1 promote tumor cell growth and were reported to enhance cell invasion. Consistently, 35 SRF/IGF2BP1-dependent genes showing conserved association with SRF and IGF2BP1 expression indicate a poor overall survival probability in ovarian, liver and lung cancer. In conclusion, these findings identify the SRF/IGF2BP1-, miRNome- and m6A-dependent control of gene expression as a conserved oncogenic driver network in cancer.
2018-10-10 | GSE116059 | GEO
Project description:The oncofetal mRNA-binding protein IGF2BP1 and the transcriptional regulator SRF modulate gene expression in cancer. In cancer cells, we demonstrate that IGF2BP1 promotes the expression of SRF in a conserved and N6-methyladenosine (m6A) dependent manner by impairing the miRNA-directed decay of the SRF mRNA. This results in enhanced SRF-dependent transcriptional activity and promotes tumor cell growth and invasion. At the post-transcriptional level, IGF2BP1 sustains the expression of various SRF-target genes. The majority of these SRF/IGF2BP1-enhanced genes, including PDLIM7 and FOXK1, shows conserved upregulation with SRF and IGF2BP1 synthesis in cancer. PDLIM7 and FOXK1 promote tumor cell growth and were reported to enhance cell invasion. Consistently, 35 SRF/IGF2BP1-dependent genes showing conserved association with SRF and IGF2BP1 expression indicate a poor overall survival probability in ovarian, liver and lung cancer. In conclusion, these findings identify the SRF/IGF2BP1-, miRNome- and m6A-dependent control of gene expression as a conserved oncogenic driver network in cancer.
2018-10-10 | GSE116133 | GEO
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