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Inhibition of the mRNA-binding protein IGF2BP1 suppresses proliferation and sensitizes neuroblastoma cells to chemotherapeutics

ABSTRACT: Inhibition of the mRNA-binding protein IGF2BP1 suppresses proliferation and sensitizes neuroblastoma cells to chemotherapeutics

PROVIDER: PRJNA664601 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12678571.fastq.gz	Fastqsanger.gz
	SRR12678571_1.fastq.gz	Fastqsanger.gz
	SRR12678571_2.fastq.gz	Fastqsanger.gz
	SRR12678572.fastq.gz	Fastqsanger.gz
	SRR12678572_1.fastq.gz	Fastqsanger.gz

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Inhibition of the mRNA-binding protein IGF2BP1 suppresses proliferation and sensitizes neuroblastoma cells to chemotherapeutics

Project description:Gain at chromosome 17q21 in neuroblastoma and is associated with a poor prognosis, independent of MYCN amplification status. Several potential proto-oncogenes have been identified in this region, one of them - insulin-like growth-factor-2 mRNA binding protein (IGF2BP1) – is expressed at high levels in stage 4 tumors, and associated with overall lower patient survival. Here, we demonstrate that down-regulation of IGF2BP1 activity, either by transcript silencing or chemical inhibition, suppresses neuroblastoma cell growth. Furthermore, the combination of IGF2BP1 inhibition along with commonly used chemotherapeutics that broadly affect DNA synthesis, or cyclin-dependent kinase (CDK) inhibitors that disrupt signal transduction, have a synergistic effect on the suppression of neuroblastoma cell proliferation.

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IGF2BP1 induces neuroblastoma via a druggable feedforward loop with MYCN promoting 17q oncogene expression [mouse sWGS]

Project description:Chromosome 17q gain is an independent prognostic marker in neuroblastoma, harboring several potential oncogenes including IGF2BP1 and BIRC5. IGF2BP1 was shown to be upregulated in unfavorable neuroblastoma and correlates with poor patient survival. Here, we report that overexpression of IGF2BP1 in a transgenic mouse model induces neuroblastoma with all characteristics known for human neuroblastoma, including MYCN upregulation and genomic aberrations. Furthermore, we demonstrate that genes located at chromosome 17q have an exceptionally high potential as therapeutic targets in addition to a combined inhibition of IGF2BP1 and BIRC5 resulting in additive effects.

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Inhibition of the mRNA-Binding Protein IGF2BP1 Suppresses Proliferation and Sensitizes Neuroblastoma Cells to Chemotherapeutic Agents.

Project description:Gain at chromosome 17q21 in neuroblastoma is associated with a poor prognosis, independent of MYCN amplification status. Several potential proto-oncogenes have been identified in this region, one of them-insulin-like growth-factor-2 mRNA binding protein (IGF2BP1)-is expressed at high levels in stage 4 tumors, and associated with overall lower patient survival. Here, we demonstrate that down-regulation of IGF2BP1 activity, either by transcript silencing or chemical inhibition, suppresses neuroblastoma cell growth. Furthermore, the combination of IGF2BP1 inhibition along with commonly used chemotherapeutics that broadly affect DNA synthesis, or cyclin-dependent kinase (CDK) inhibitors that disrupt signal transduction, have a synergistic effect on the suppression of neuroblastoma cell proliferation.

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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.

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Tumor suppressive function of IGF2BP1 in gastric cancer through decreasing MYC

Project description:Gastric cancer is one of the most common causes of cancer-related death worldwide. The N6-methyladenosine (m6A) reader IGF2BP1 (insulin-like growth factor-2 mRNA binding protein 1) has been reported to promote cancer progression by stabilizing oncogenic mRNAs through its m6A-binding activity in some tumors. However, the role of IGF2BP1 in gastric carcinogenesis remains unclear. In this study, we find that IGF2BP1 is significantly downregulated in tumor tissues from patients with gastric cancer. Lower expression of IGF2BP1 is associated with poor prognosis. IGF2BP1 suppresses gastric cancer cell proliferation in an m6A-dependent manner. Additionally, IGF2BP1 is able to significantly attenuate tumor growth of gastric cancer cells. Further m6A sequencing and m6A-RIP (RNA immunoprecipitation) assays show that MYC (c-myc proto-oncogene) mRNA is a target transcript of IGF2BP1 in gastric cancer cells. IGF2BP1 inhibits gastric cancer cell proliferation by reducing the mRNA and protein expression of MYC. Mechanistically, IGF2BP1 promotes the degradation of MYC mRNA and inhibits its translation efficiency. Taken together, these data suggest that IGF2BP1 plays a tumor-suppressive role in gastric carcinogenesis by downregulating MYC in an m6A-dependent manner, thereby making the IGF2BP1-MYC axis a potential target for gastric cancer treatment.

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