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ABSTRACT: CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A modified CREB1 mRNA

PROVIDER: PRJNA843182 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19434825.fastq.gz	Fastqsanger.gz
	SRR19434826.fastq.gz	Fastqsanger.gz
	SRR19434827.fastq.gz	Fastqsanger.gz
	SRR19434828.fastq.gz	Fastqsanger.gz
	SRR19434829.fastq.gz	Fastqsanger.gz

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CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A modified CREB1 mRNA

Project description:CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A modified CREB1 mRNA

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Project description:CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A modified CREB1 mRNA

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Project description:CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A-modified CREB1 mRNA

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CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A modified CREB1 mRNA [miRNA-seq]

Project description:Background: Aberrant expression of circular RNAs contributes to the initiation and progression of human malignancies, but the underlying mechanisms remain largely elusive. Methods: High throughput sequencing was performed to screen aberrantly expressed circRNAs or miRNAs in colorectal cancer and adjacent normal tissues. A series of gain and loss of function studies were conducted to evaluate the biological behaviors of CRC cells. RNA pulldown, mass spectrometry, RIP, qRT PCR, western blot, luciferase reporter assays and MeRIP seq analysis were further applied to dissect the detailed mechanisms. Results: Here, a novel circRNA named circEZH2 , was screened out by RNA seq in CRC tissues, whose expression is related to clinicpathological characteristics and prognosis in CRC patients. Biologically, circEZH2 facilitates the proliferation and migration of CRC cells in vitro and in vivo. Mechanistically, circEZH2 interacts with m6A reader IGF2BP2 and blocks its ubiquitination dependent degradation. Meanwhile, circEZH2 could serve as a competing endogenous RNA for miR 133b, resulting in the upregulation of IGF2BP2. Particularly, circEZH2 IGF2BP2 enhances the stability of CREB1 mRNA, thus aggravating CRC progression. Conclusions: Our findings not only reveal the pivotal roles of circEZH2 in modulating CRC progression, but also advocate for attenuating circEZH2 miR 133b IGF2BP2 CREB1 regulatory axis to combat CRC.

2022-06-04 | GSE205094 | GEO

CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A modified CREB1 mRNA [circRNA-seq]

2022-06-04 | GSE205241 | GEO

Landscape of m6A modification in haematopoietic system unveils an essential role of IGF2BP2 in preserving haematopoietic stem cell function

Project description:N6-methyladenosine (m6A) is an abundant modification on mRNA, and plays critical functions in various cellular processes, including cell fate determination and lineage transition. However, the landscape and dynamics of m6A modification in haematopoietic system remain unknown. Here, we delineate a comprehensive m6A landscape across haematopoietic hierarchy and uncover that IGF2BP2 is required for preserving haematopoietic stem cells (HSCs) function. Our data reveal a marked cell-type- and haematopoietic-lineage-specific m6A landscape. Intriguingly, most m6A modifications arise in the early stat of haematopoiesis, and are critical in defining cellular states of HSCs. Moreover, m6A modification is the major factor in determining mRNA abundance in HSCs. Importantly, we find that higher expression of m6A reader IGF2BP2 is critical in controlling gene expression states and the functional maintenance of HSCs. IGF2BP2 deficiency induces apoptosis and quiescence loss, and substantially impairs the reconstitution capacity of HSCs. In addition, deletion of IGF2BP2 increases the mitochondrial activity of HSCs. Mechanistically, IGF2BP2 stabilizes Bmi1 mRNA in an m6A-dependent manner, which represses the expression of mitochondria-related genes. Collectively, our results present a fascinating portrait of m6A modification during haematopoiesis, and uncover a key role of IGF2BP2 in maintaining HSCs function by regulating Bmi1 stability and restraining mitochondrial activity.

2021-10-26 | GSE165863 | GEO

Comprehensive analysis of differentially expressed profiles of mRNA N6-methyladenosine in colorectal cancer

Project description:Purpose: To comprehensively profile the landscape of the mRNA N6-methyladenosine (m6A) modification in human colorectal cancer (CRC). Methylated RNA immunoprecipitation sequencing (MeRIP-seq) was explored to compare the difference in mRNA N6-methyladenosine (m6A) methylation between CRC tissues and adjacent normal control (NC) tissue. RNA-sequencing (RNA-seq) was performed to transcribe differentially expressed mRNAs. Conjoint analysis of MeRIP-seq and RNA-seq data was conducted to predict RNA-binding proteins (RBPs). Results: MeRIP-seq identified 1110 differentially m6A methylated sites (DMMSs) and 980 differentially m6A methylated genes (DMMGs) in CRC, with 50.13% of all modified genes showing unique m6A-modified peaks in CRC. RNA-seq showed 915 upregulated genes and 1463 downregulated genes in CRC. QRT-PCR verified the RNA-seq results by detecting the expression of some mRNAs. Conjoint analysis of MeRIP-seq and RNA-seq identified 400 differentially m6A methylated and expressed genes (DEGs), and pathway analysis detected that DMMGs and DEGs were closely related to cancer. After analyzing these DMMGs and DEGs through the GEPIA database, we found that the expression of B3GNT6, DKC1, SRPK1 and RIMKLB were associated with prognosis, and the expression of B3GNT6 and RIMKLB were associated with clinical stage. 17 RBPs were identified based on the DMMGs and DEGs, among which FXR1, FXR2, FMR1, IGF2BP2, IGF2BP3 and SRSF1 were obviously highly expressed in CRC, and FMR1, IGF2BP2 and IGF2BP3 were closely related to methylation, and might be involved in the development of CRC. Conclusions: This study comprehensively profiled m6A modification of mRNAs in CRC, which revealed possible mechanisms of m6A-mediated gene expression regulation.

2022-02-02 | GSE190388 | GEO

DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [m6A-seq]

Project description:DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [m6A-seq]

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Inhibition of the m6A Reader IGF2BP2 as a Strategy against T-cell Acute Lymphoblastic Leukemia

Project description:N6-methyladenosine (m6A) reader Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) participates in the initiation and growth of cancers by communicating with various targets. Here, we found IGF2BP2 is highly expressed in T-ALL. Gain and loss of IGF2BP2 demonstrated IGF2BP2 was essential for T-ALL cell proliferation in vitro and loss of IGF2BP2 prolonged animal survival in a human T-ALL xenograft model. Mechanistically, IGF2BP2 directly bound to T-ALL oncogene NOTCH1 via an m6A dependent manner.

2022-09-15 | GSE205503 | GEO

m6A-modified CBX1 regulates NPC progression.

Project description:m6A-modified CBX1 regulates NPC progression.

| PRJNA826827 | ENA