IGF2BP2 promotes the progression of colorectal cancer through a YAP‐dependent mechanism

Cui, Jie; Tian, Jiale; Wang, Weiwei; He, Tao; Li, Xin; Gu, Chenzheng; Wang, Lixin; Wu, Jian; Shang, Anquan

doi:10.1111/cas.15083

Cited by 53 publications

(32 citation statements)

References 43 publications

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“…Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) belongs to an evolutionally conserved family of RNA-binding proteins, including IGF2BP1, IGF2BP2 and IGF2BP3 in human eukaryotic cells. IGF2BP2 dysregulation is frequently observed and plays a key tumor-promoting role in various malignancies, especially in CRC [ 34 , 35 ]. However, little is known about the post-transcriptionally regulation of IGF2BP2 protein.…”

Section: Discussionmentioning

confidence: 99%

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

Yao

Yang

et al. 2022

Mol Cancer

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Background Aberrant expression of circular RNAs (circRNAs) 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 (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. Results Here, 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. 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.

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Section: Discussionmentioning

confidence: 99%

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

Yao

Yang

et al. 2022

Mol Cancer

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“…IGF2BP2 overexpression promotes the proliferation and directly recognizes the m 6 A site on FEN1 mRNA to enhance FEN1 mRNA stability [ 20 ]. In colorectal cancer, IGF2BP2 promotes the proliferation, invasion, and migration of cancer cells through activating the expression of ErbB2 by recognizing the m 6 A of YAP [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

N⁶-methyladenosine (m⁶A) reader IGF2BP2 promotes gastric cancer progression via targeting SIRT1

et al. 2022

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N 6 -methyladenosine (m 6 A) modification acts as the most prevalent internal modification in eukaryotic mRNA. Emerging evidence shows the critical biological roles of m 6 A key enzymes in human cancers. However, the roles of m 6 A binding protein IGF2BP2 in gastric cancer (GC) progression are still unclear. In this study, we confirmed that IGF2BP2 was highly expressed in GC cell lines and tumor tissues. Knocking down of IGF2BP2 suppressed cell proliferation and migration, and repressed xenograft tumor growth in vivo, while IGF2BP2 overexpression promoted the proliferation and migration. Mechanistically, we identified that IGF2BP2 regulated GC the proliferation/migration through recognizing the m 6 A modification sites of SIRT1 mRNA. In general, our findings demonstrated a novel regulatory mechanism that IGF2BP2/SIRT1 axis modulated GC progression in an m 6 A-dependent manner, suggesting that m 6 A may be a therapeutic target for GC.

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“…For example, higher expression of IGF2BP2 is associated with a poorer prognosis in HCC patients, and mechanistically, IGF2BP2 directly recognizes and binds to the m 6 A site of flap endonuclease-1 (FEN1), and maintains its mRNA expression 92 . Analogously, in colorectal cancer, IGF2BP2 recognizes and binds to m 6 A-modified YAP and enhances the stability of YAP mRNA, thereby facilitating tumorigenesis 163 . Similarly, IGF2BP2 recognizes the coding sequence (CDS) regions of transcription factor SOX2 and protects it from degradation in m 6 A- mediated manner, which facilitates tumorigenesis and metastasis in colorectal cancer 164 .…”

Section: The Role Of Igf2bps As M 6 a Reader In Ca...mentioning

confidence: 99%

The role of Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) as m⁶A readers in cancer

Sun¹,

Cao²,

Du³

et al. 2022

Int. J. Biol. Sci.

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RNA can be modified by over 170 types of distinct chemical modifications, and the most abundant internal modification of mRNA in eukaryotes is N6-methyladenosine (m 6 A). The m 6 A modification accelerates mRNA process, including mRNA splicing, translation, transcript stability, export and decay. m 6 A RNA modification is installed by methyltransferase-like proteins (writers), and potentially removed by demethylases (erasers), and this process is recognized by m 6 A-binding proteins (readers). Notably, alterations of m 6 A-modified proteins (writers, erasers and readers) are involved in the tumorigenesis, progression and metastasis. Importantly, the fate of m 6 A-methylated mRNA is mediated mostly through m 6 A readers, and among these readers, insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) are unique RNA-binding proteins (RBPs) that stabilize their targets mRNA via m 6 A modification. In this review, we update the writers, erasers and readers, and their cross-talks in m 6 A modification, and briefly discuss the oncogenic role of IGF2BPs in cancer. Most importantly, we mainly review the up-to-date knowledges of IGF2BPs (IGF2BP1/2/3) as m 6 A readers in an m 6 A-modified manner in cancer progression.

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IGF2BP2 promotes the progression of colorectal cancer through a YAP‐dependent mechanism

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Cited by 53 publications

References 43 publications

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

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

N⁶-methyladenosine (m⁶A) reader IGF2BP2 promotes gastric cancer progression via targeting SIRT1

The role of Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) as m⁶A readers in cancer

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IGF2BP2 promotes the progression of colorectal cancer through a YAP‐dependent mechanism

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Cited by 53 publications

References 43 publications

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

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

N6-methyladenosine (m6A) reader IGF2BP2 promotes gastric cancer progression via targeting SIRT1

The role of Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) as m6A readers in cancer

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N⁶-methyladenosine (m⁶A) reader IGF2BP2 promotes gastric cancer progression via targeting SIRT1

The role of Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) as m⁶A readers in cancer