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IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [RNA-seq]

ABSTRACT: Combination analysis of m6A-seq, IGF2BP1-KD RNA-seq, IGF2BP1 CLIP-seq in H929 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE202974 | GEO | 2024/05/31

REPOSITORIES: GEO

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IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way [CLIP-seq]

Project description:Combination analysis of m6A-seq, IGF2BP1-KD RNA-seq, IGF2BP1 CLIP-seq in H929 cells

2024-05-31 | GSE202973 | GEO

IGF2BP1 regulate proliferation of multiple myeloma with chromosome 1q gain via CDC5L in a M6A way

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-31 | GSE202975 | GEO

m6A modification profile in primary microglia with/without Igf2bp1 knockdown

Project description:Our study demonstrated that the expression of Igf2bp1 in activated microglia was significantly up-regulated, implying a role of Igf2bp1 in LPS-induced m6A modifications in microglia. To understand the roles of Igf2bp1 on LPS-induced m6A modification in microglia, we performed Igf2bp1 loss-of-function (LOF) approach. Microglia stimulated by LPS were transfected with either scrambled siRNA control or Igf2bp1 siRNA for 48 hours. To m6A modification profiles in control and Igf2bp1 LOF microglia were determined by MeRIP-seq analysis.

2022-12-31 | E-MTAB-11411 | biostudies-arrayexpress

IGF2BP1 enhances an aggressive tumor cell phenotype by impairing miRNA-directed downregulation of oncogenic factors [mRNA]

Project description:The oncofetal IGF2 mRNA binding protein (IGF2BP) family modulates tumor cell properties but IGF2BP paralogue-specific roles remain poorly understood. We demonstrate that phenotypic roles of IGF2BPs vary in a cancer cell-dependent manner. However, only IGF2BP1 shows oncogenic potential in all cancer cells analyzed. Consistently, only IGF2BP1 expression is associated with poor prognosis in ovarian carcinoma and promotes all oncogenic properties analyzed in ovarian cancer-derived tumor cells. Despite a substantial overlap of candidate target mRNAs of IGF2BP paralogues proposed by CLIP analyses, the paralogue-specific depletion of IGF2BPs induces strikingly distinct deregulation of mRNA abundance. Transcripts decreased by IGF2BP1 depletion or knockout are enriched for IGF2BP1- as well as AGO-CLIP hits conserved in distinct cell lines, are prone to targeting by highly abundant miRNAs and comprise significantly longer 3’UTRs. Downregulation of target mRNAs upon IGF2BP1 depletion is abrogated when miRNAs are expressed at low levels or depleted by DICER/DROSHA knockdown. Strikingly, the depletion of all 12 randomly selected miRNA-prone target mRNAs impairs at least one analyzed IGF2BP1-modulated tumor cell property. These findings indicate that IGF2BPs serve distinct roles in cancer-derived cells and suggest that IGF2BP1’s main role is the post-transcriptional, miRNome-dependent enhancement of factors promoting oncogenic tumor cell properties.

2018-03-19 | GSE109604 | GEO

IGF2BP1 enhances an aggressive tumor cell phenotype by impairing miRNA-directed downregulation of oncogenic factors [small RNA]

Project description:The oncofetal IGF2 mRNA binding protein (IGF2BP) family modulates tumor cell properties but IGF2BP paralogue-specific roles remain poorly understood. We demonstrate that phenotypic roles of IGF2BPs vary in a cancer cell-dependent manner. However, only IGF2BP1 shows oncogenic potential in all cancer cells analyzed. Consistently, only IGF2BP1 expression is associated with poor prognosis in ovarian carcinoma and promotes all oncogenic properties analyzed in ovarian cancer-derived tumor cells. Despite a substantial overlap of candidate target mRNAs of IGF2BP paralogues proposed by CLIP analyses, the paralogue-specific depletion of IGF2BPs induces strikingly distinct deregulation of mRNA abundance. Transcripts decreased by IGF2BP1 depletion or knockout are enriched for IGF2BP1- as well as AGO-CLIP hits conserved in distinct cell lines, are prone to targeting by highly abundant miRNAs and comprise significantly longer 3’UTRs. The downregulation of target mRNAs observed upon IGF2BP1 depletion is abrogated when miRNAs are expressed at low levels or depleted by DICER/DROSHA knockdown. Strikingly, the depletion of 10 randomly selected miRNA-prone target mRNAs impairs at least one analyzed IGF2BP1-modulated tumor cell property. These findings indicate that IGF2BPs serve distinct roles in cancer-derived cells and suggest that IGF2BP1’s main role is the post-transcriptional, miRNome-dependent enhancement of factors promoting oncogenic tumor cell properties.

2018-03-19 | GSE109422 | GEO

IGF2BP1 enhances an aggressive tumor cell phenotype by impairing miRNA-directed downregulation of oncogenic factors [HUH-7 small RNA]

2018-03-19 | GSE109677 | GEO

RNA-Seq of circCDYL knockdown (KD) samples in HepG2, J82, and UMUC3 cells and of GRWD1, IGF2BP1, and IGF2BP2 knockdown (KD) samples in J82 and UMUC3 cells

Project description:We profile gene expression upon circCDYL KD in HepG2 cells and in two bladder cancer cell lines J82 and UMUC3 as well as upon knockdown of the RNA binding proteins (RBP) GRWD1, IGF2BP1, and IGF2BP2 in J82 and UMUC3

2020-11-11 | GSE146726 | GEO

IGF2BP1 promotes SRF-dependent transcription in cancer in a m6A- and miRNA-dependent manner [IGF2BP1 and SRF KD in ES-2 (total RNA)]

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

Identify mRNAs binding with IGF2BP1 in PLC-8024 cells [RIP-seq]

Project description:To investigate mRNAs binding with IGF2BP1 in HCC, we employed the RIP-seq

2023-02-28 | GSE206504 | GEO

IGF2BP1 is a druggable, post-transcriptional super-enhancer of E2F-driven gene expression hallmark in cancer [IGF2BP1 KD in MV3 (total 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.

2020-06-17 | GSE146803 | GEO

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