CRD-BP shields c-myc and MDR-1 RNA from endonucleolytic attack by a mammalian endoribonuclease

Sparanese, Dan; Lee, Chow H.

doi:10.1093/nar/gkl1148

Cited by 74 publications

(108 citation statements)

References 41 publications

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“…Moreover, the knockdown of IMP1 led to reduced luciferase activity expressed from a reporter construct comprising the c-myc CRD-element (coding region determinant) in frame to the luciferase coding sequence, whereas a control reporter lacking the CRD region remained unaffected by the knockdown of IMP1 (Supplementary Figure S3). Hence, IMP1 was confirmed to be essential for controlling c-myc mRNA turnover via the CRD-element located in the coding region of the c-myc mRNA, as suggested previously (Lemm and Ross, 2002;Sparanese and Lee, 2007).…”

supporting

confidence: 74%

Expression of the RNA-binding protein IMP1 correlates with poor prognosis in ovarian carcinoma

et al. 2007

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The IMP (IGFII mRNA-binding protein) family comprises a group of three RNA-binding proteins involved in the regulation of cytoplasmic mRNA-fate. Recent studies identified IMP proteins as oncofetal factors in various neoplasias, but knowledge of a potential role in ovarian carcinomas is still lacking. The immunohistochemical analysis of 107 ovarian carcinomas, 30 serous borderline tumors of the ovary and five normal ovaries revealed de novo synthesis of IMP1 in 69% of ovarian carcinomas. Elevated IMP1 expression was observed preferentially in high-grade and high-stage cases and was a significant prognostic indicator for reduced recurrence-free and overall survival. Phenotypic studies in ovarian carcinoma-derived ES-2 cells demonstrated that IMP1 knockdown affects proliferation and cell survival. Reduced proliferation was associated with decreased c-myc mRNA half-life, suggesting IMP1 as an oncogenic factor that is involved in promoting elevated proliferation by stabilizing the c-myc mRNA in ovarian carcinoma cells.

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confidence: 74%

Expression of the RNA-binding protein IMP1 correlates with poor prognosis in ovarian carcinoma

et al. 2007

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“…As described previously, the binding of IGF2BP1 to c-MYC and MKI67 mRNA prevented mRNA degradation and increased mRNA expression (17)(18)(19); the stabilization of CD44 mRNA was attributed to the 3Ј-UTR of the transcript, which was bound by IGF2BP1 protein (20); PTEN mRNA was identified as a novel target transcript of IGF2BP1 and decayed faster in cells upon IGF2BP1 knockdown (21). To verify that the down-regulation of IGF2BP1 expression due to the up-regulation of miR-873 in GBM cells could destabilize c-MYC, MKI67, CD44, and PTEN mRNA, we measured the mRNA levels of these potential target transcripts of IGF2BP1.…”

Section: High Level Of Mir-873 Decreased the Mrna Level Of Mki67 C-mmentioning

confidence: 64%

MicroRNA-873 (MiRNA-873) Inhibits Glioblastoma Tumorigenesis and Metastasis by Suppressing the Expression of IGF2BP1

Wang

Bao

et al. 2015

Journal of Biological Chemistry

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Background: Recent research has uncovered tumor-suppressive and oncogenic potential of miRNAs. Results: miR-873 suppresses the proliferation, migration, and invasiveness of GBM cells by targeting IGF2BP1. Conclusion: Down-regulation of miR-873 results in overexpressed IGF2BP1, contributing to tumorigenesis of GBM cells. Significance: The identification of tumor suppressor miR-873 and its oncogenic target IGF2BP1 in GBM cells is potentially valuable for cancer diagnosis and therapy.

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“…Coding region determinant-binding protein is a multifunctional mRNA-binding protein, which was shown to modulate the stability, localization and translation of several RNAs (c-myc, IGF-II, H19, bTrCP1, CD4, MDR-1, and so on) (Prokipcak et al, 1994;Nielsen et al, 1999;Runge et al, 2000;Noubissi et al, 2006;Vikesaa et al, 2006;Sparanese and . CRD-BP belongs to a conserved VICKZ family of mRNA-binding proteins, characterized by the presence of four hnRNP K-homology domains and two RNA recognition motifs (Doyle et al, 1998).…”

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confidence: 99%

Overexpression of mRNA-binding protein CRD-BP in malignant melanomas

et al. 2008

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Wnt/b-catenin signaling pathway plays an important role in embryogenesis, stem cell maintenance, tumorigenesis and aging. Here, we show that RNA-binding protein, coding region determinant-binding protein (CRD-BP) (a transcriptional target of Wnt signaling pathway), is highly expressed in primary human malignant melanomas and melanoma cell lines with activated Wnt/b-catenin signaling pathway. Upregulation of CRD-BP is associated with an elevated level of b-TrCP1 ubiquitin ligase receptor and activation of nuclear transcriptional factors-kappa B (NF-jB) signaling. Knockdown of CRD-BP inhibits NF-jB activity, induces apoptosis, and suppresses proliferation and tumorigenic properties of melanoma cells. Keywords: CRD-BP; b-TrCP; mRNA stability; melanoma; Wnt/b-catenin signaling; NF-kB The increased incidence of cutaneous melanoma in the past three decades, its highly progressive nature and resistance to treatment, has prompted enhanced attention to this disease (reviewed in Chin et al., 2006;Herlyn, 2006). Despite numerous studies conducted on melanocytic lesions, the molecular mechanisms of melanoma development and progression are still poorly understood.Wnt/b-catenin signaling plays an important role in normal development and stem cells maintenance, whereas its aberrant upregulation is involved in tumorigenesis (Giles et al., 2003;Weeraratna, 2005). The defining events of an active canonical Wnt pathway include accumulation of cytoplasmic b-catenin, its subsequent nuclear translocation and initiation of bcatenin/Tcf-dependent transcription. In the absence of WNT, abundance and transcriptional activity of b-catenin is regulated by the large multicomponent machinery that includes adenomatous polyposis coli protein (APC), axin, CK1 and glycogen synthase kinase 3-b. This complex facilitates phosphorylation of bcatenin and determines its subsequent degradation. Binding of WNT ligand with its Frizzled and lowdensity lipoprotein receptor-related protein (5/6) receptors starts a cascade of events that results in disruption of b-catenin phosphorylation, subsequent accumulation of free b-catenin in the cytoplasm, its nuclear translocation and transcriptional activation of target genes. Overexpression of WNT proteins, mutations in APC and/or stabilizing b-catenin mutations are the most common alterations associated with constitutively upregulated Wnt signaling and tumor development. Nuclear localization of b-catenin, the hallmark of an active canonical Wnt pathway, was observed in approximately 30% of primary and metastatic human melanoma samples (Rimm et al., 1999).Activation of nuclear transcriptional factors-kappa B (NF-kB) is frequently observed in various types of human tumors, including melanoma (Basseres and Baldwin, 2006;Gilmore, 2006). In many cells, the major NF-kB heterodimer is composed of p50 and RelA/p65 subunits that are responsible for activation of canonical NF-kB signaling. The inhibitors of NF-kB (IkBs) tightly regulate activity of p50/RelA dimer. The IkBs bind to NF-kB dimers and block their nuclear locali...

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CRD-BP shields c-myc and MDR-1 RNA from endonucleolytic attack by a mammalian endoribonuclease

Cited by 74 publications

References 41 publications

Expression of the RNA-binding protein IMP1 correlates with poor prognosis in ovarian carcinoma

Expression of the RNA-binding protein IMP1 correlates with poor prognosis in ovarian carcinoma

MicroRNA-873 (MiRNA-873) Inhibits Glioblastoma Tumorigenesis and Metastasis by Suppressing the Expression of IGF2BP1

Overexpression of mRNA-binding protein CRD-BP in malignant melanomas

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