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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE205242 | GEO | 2022/06/04

REPOSITORIES: GEO

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CircEZH2 miR-133b IGF2BP2 aggravates colorectal cancer progression via enhancing the stability of m6A modified CREB1 mRNA [circRNA-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 | GSE205241 | GEO

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

2022-06-04 | GSE205094 | GEO

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

Project description: Not available

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LINC00460/DHX9/IGF2BP2 complex promotes colorectal cancer proliferation and metastasis by mediating HMGA1 mRNA stability depending on m6A modification.

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

Project description:Both N6-methyladenosine (m6A) mediates RNA fates and ubiquitin mediates protein fates play an important role in either physiology or pathology including cancer, yet how long noncoding RNAs (lncRNAs) are involved in a link of molecular fate between m6A and ubiquitin remains unknown. Here, we reveal a role for a lncRNA Downregulated RNA in Cancer (DRAIC) to suppress tumor growth and metastasis in clear cell Renal Carcinoma (ccRCC). Mechanistically, DRAIC physically interacts with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) and enhances its protein stability by blocking E3 ligase F-box protein 11 (FBXO11)-mediated ubiquitin and proteasome-dependent degradation. Subsequently, hnRNPA2B1 destabilizes m6A modified-type 1 insulin-like growth factor receptor (IGF1R) to lead to inhibition of ccRCC progression. Moreover, four m6A modification sites of IGF1R are identified and results in its mRNA degradation. Collectively, our findings reveal that DRAIC/hnRNPA2B1 axis regulates IGF1R mRNA expression in an m6A-dependent manner and highlights an important mechanism of IGF1R fate. These findings shed light on DRAIC/hnRNPA2B1/FBXO11/IGF1R axis as potential therapeutic targets in ccRCC and build a link of molecular fate between m6A-modified RNA and ubiquitin-modified protein.

2024-01-07 | GSE244892 | GEO

RNA m6A reader IMP2/IGF2BP2 promotes pancreatic β-cell proliferation and insulin secretion by enhancing PDX1 expression.

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

2024-04-26 | GSE262500 | GEO