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

Köbel, Martin; Weidensdorfer, D; Reinke, Claudia; Lederer, Marcell; Schmitt, Wolfgang; Zeng, Katharina; Thomssen, Christoph; Hauptmann, Steffen; Hüttelmaier, Stefan

doi:10.1038/sj.onc.1210563

Cited by 107 publications

(129 citation statements)

References 24 publications

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“…IGF2BP1 is expressed during embryogenesis, but this protein is also synthesized in a broad variety of malignancies (33). The expression of IGF2BP1 was associated with an overall poor prognosis in a wide range of cancers, suggesting that the protein may act as a potent oncogenic factor (34,35). Accordingly, we observed that IGF2BP1 expression was up-regulated in tumor tissue (Fig.…”

Section: Discussionsupporting

confidence: 50%

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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Section: Discussionsupporting

confidence: 50%

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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“…In addition, the survival and proliferation genes CDC25A, Myc, and Src, which we identified as indirect downstream targets for triptolide, have previously been identified as important oncogenic regulators of acute myeloid leukemia (46)(47)(48). Myc has also been described to be directly involved in the tumorigenicity of ovarian, colon, and esophageal cancers (48)(49)(50)(51). Altogether, these results represent a breakthrough toward the potential therapeutic benefits from a triptolide-based therapy in cancer.…”

Section: Discussionmentioning

confidence: 54%

Triptolide is an inhibitor of RNA polymerase I and II–dependent transcription leading predominantly to down-regulation of short-lived mRNA

Vispé

DeVries

Créancier

et al. 2009

Molecular Cancer Therapeutics

159

135

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Triptolide, a natural product extracted from the Chinese plant Tripterygium wilfordii, possesses antitumor properties. Despite numerous reports showing the proapoptotic capacity and the inhibition of NF-κB-mediated transcription by triptolide, the identity of its cellular target is still unknown. To clarify its mechanism of action, we further investigated the effect of triptolide on RNA synthesis in the human non-small cell lung cancer cell line A549. Triptolide inhibited both total RNA and mRNA de novo synthesis, with the primary action being on the latter pool. We used 44K human pan-genomic DNA microarrays and identified the genes primarily affected by a short treatment with triptolide. Among the modulated genes, up to 98% are down-regulated, encompassing a large array of oncogenes including transcription factors and cell cycle regulators. We next observed that triptolide induced a rapid depletion of RPB1, the RNA polymerase II main subunit that is considered a hallmark of a transcription elongation blockage. However, we also show that triptolide does not directly interact with the RNA polymerase II complex nor does it damage DNA. We thus conclude that triptolide is an original pharmacologic inhibitor of RNA polymerase activity, affecting indirectly the transcription machinery, leading to a rapid depletion of short-lived mRNA, including transcription factors, cell cycle regulators such as CDC25A, and the oncogenes MYC and Src. Overall, the data shed light on the effect of triptolide on transcription, along with its novel potential applications in cancers, including acute myeloid leukemia, which is in part driven by the aforementioned oncogenic factors. [Mol Cancer Ther 2009;8(10):2780-90]

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“…Members of the protein family show an oncofetal expression declining toward the end of embryogenesis, barely detectable expression in the postnatal phase, but rapid de novo synthesis in various neoplasias (Nielsen et al 1999;Yaniv and Yisraeli 2002;Kobel et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Control of c-myc mRNA stability by IGF2BP1-associated cytoplasmic RNPs

Weidensdorfer¹,

Stöhr²,

Baude³

et al. 2008

RNA

284

288

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The RNA-binding protein IGF2BP1 (IGF-II mRNA binding protein 1) stabilizes the c-myc RNA by associating with the Coding Region instability Determinant (CRD). If and how other proteins cooperate with IGF2BP1 in promoting stabilization of the cmyc mRNA via the CRD remained elusive. Here, we identify various RNA-binding proteins that associate with IGF2BP1 in an RNA-dependent fashion. Four of these proteins (HNRNPU, SYNCRIP, YBX1, and DHX9) were essential to ensure stabilization of the c-myc mRNA via the CRD. These factors associate with IGF2BP1 in a CRD-dependent manner, co-distribute with IGF2BP1 in non-polysomal fractions comprising c-myc mRNA, and colocalize with IGF2BP1 in the cytoplasm. A selective shift of relative c-myc mRNA levels to the polysomal fraction is observed upon IGF2BP1 knockdown. These findings suggest that IGF2BP1 in complex with at least four proteins promotes CRD-mediated mRNA stabilization. Complex formation at the CRD presumably limits the transfer of c-myc mRNA to the polysomal fraction and subsequent translation-coupled decay.

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

Cited by 107 publications

References 24 publications

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

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

Triptolide is an inhibitor of RNA polymerase I and II–dependent transcription leading predominantly to down-regulation of short-lived mRNA

Control of c-myc mRNA stability by IGF2BP1-associated cytoplasmic RNPs

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