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

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

PROVIDER: PRJNA844242 | ENA |

REPOSITORIES: ENA

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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

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

| PRJNA843182 | ENA

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

| PRJNA843315 | ENA

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

| PRJNA842955 | ENA

CircEZH2/miR-133b/IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m<sup>6</sup>A-modified CREB1 mRNA.

Project description:BackgroundAberrant expression of circular RNAs (circRNAs) contributes to the initiation and progression of human malignancies, but the underlying mechanisms remain largely elusive.MethodsHigh-throughput sequencing was performed to screen aberrantly expressed circRNAs or miRNAs in colorectal cancer (CRC) 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.ResultsHere, a novel circRNA named circEZH2 (hsa_circ_0006357) was screened out by RNA-seq in CRC tissues, whose expression is closely related to the clinicpathological characteristics and prognosis of 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 sponge of miR-133b, resulting in the upregulation of IGF2BP2. Particularly, circEZH2/IGF2BP2 enhances the stability of CREB1 mRNA, thus aggravating CRC progression.ConclusionsOur 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.

| S-EPMC9245290 | biostudies-literature

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

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

2022-06-04 | GSE205242 | GEO

IMP2/IGF2BP2 HITS-CLIP from E13.5 mouse brain

Project description:HITS-CLIP is performed for the RNA-binding protein, IMP2/IGF2BP2, from E13.5 mouse brain.

2016-06-06 | E-MTAB-3636 | biostudies-arrayexpress

Hepatocyte-specific knock-out of Nfib aggravates hepatocellular tumorigenesis via enhancing urea cycle

Project description:Hepatocyte-specific knock-out of Nfib aggravates hepatocellular tumorigenesis via enhancing urea cycle

| PRJNA826111 | ENA

Igf2bp2 deletion reduces energy metabolism, gIgf2bp2 deletion reduces energy metabolism, growth signaling, and aging of hematopoietic stem cells in micerowth signaling, and aging of hematopoietic stem cells in mice

Project description:Increasing evidence links metabolic activity and cell growth to decline in hematopoietic stem cell (HSC) function during aging. The Lin28b/Hmga2 pathway controls tissue development and in the hematopoietic system the postnatal downregulation of this pathway causes a decrease in self renewal of adult HSCs compared to fetal HSCs. Igf2bp2 is an RNA binding protein and a mediator of the Lin28b/Hmga2 pathway, which regulates metabolism and growth signaling by influencing RNA stability and translation of its target genes. It is currently unknown whether Lin28/Hmga2/Igf2bp2 signaling impacts on aging-associated impairments in HSC function and hematopoiesis. Here, we analyzed homozygous Igf2bp2 germline knockout mice and wildtype control animals to address this question. The study shows that Igf2bp2 deletion rescues aging phenotypes of the hematopoietic system, such as the expansion of HSC numbers in bone marrow and the biased increase of myeloid cells in peripheral blood. This rescue of hematopoietic aging coincides with reduced mitochondrial metabolism and glycolysis in Igf2bp2-/- HSCs compared to Igf2bp2+/+ HSCs. Conversely, Igf2bp2 overexpression activates protein synthesis pathways in HSCs and leads to a rapid loss of self renewal by enhancing myeloid skewed differentiation in an mTOR/PI3K-dependent manner. Together, these results show that Igf2bp2 regulates energy metabolism and growth signaling in HSCs and that the activity of this pathways influences self renewal, differentiation, and aging of HSCs.

2024-05-21 | PXD018535 | Pride

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