The IGF2BP2-lncRNA TRPC7-AS1 axis promotes hepatocellular carcinoma cell proliferation and invasion

Zhang, Xu; Li, Zilin; Nie, Huizong; Huang, Yue; Du, Jingyang; Xi, Yiling; Guo, Chaoqin; Mu, Mingshan; Li, Xiangyu; Zheng, Xiaoliang; Xu, Qiuran; Huang, Dongsheng; Tu, Linglan; Cheng, Liyan

doi:10.1016/j.cellsig.2024.111078

Cited by 5 publications

References 33 publications

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Zika virus remodels and hijacks IGF2BP2 ribonucleoprotein complex to promote viral replication organelle biogenesis

Mazeaud,

Pfister,

Owen

et al. 2023

Preprint

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SUMMARYZika virus (ZIKV) infection causes significant human disease that, with no approved treatment or vaccine, constitutes a major public health concern. Its life cycle entirely relies on the cytoplasmic fate of the viral RNA genome (vRNA) through a fine-tuned equilibrium between vRNA translation, replication and packaging into new virions, all within virus-induced replication organelles (vRO). In this study, with an RNAi mini-screening and subsequent functional characterization, we have identified insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) as a new host dependency factor that regulates vRNA synthesis. In infected cells, IGF2BP2 associates with viral NS5 polymerase and redistributes to the perinuclear viral replication compartment. Combined fluorescencein situhybridization-based confocal imaging,in vitrobinding assays, and immunoprecipitation coupled to RT-qPCR, showed that IGF2BP2 directly interacts with ZIKV vRNA 3’-nontranslated region. Using ZIKV sub-genomic replicons and a replication-independent vRO induction system, we demonstrated that IGF2BP2 knockdown impairsde novoviral organelle biogenesis and, consistently, vRNA synthesis. Finally, the analysis of immunopurified IGF2BP2 complex using quantitative mass spectrometry and RT-qPCR, revealed that ZIKV infection alters the protein and RNA interactomes of IGF2BP2. Altogether, our data support that ZIKV hijacks and remodels the IGF2BP2 ribonucleoprotein complex to regulate vRO biogenesis and vRNA neosynthesis.

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Zika virus remodels and hijacks IGF2BP2 ribonucleoprotein complex to promote viral replication organelle biogenesis

Mazeaud,

Pfister,

Owen

et al. 2023

Preprint

View full text Add to dashboard Cite

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The Emerging Role of IGF2BP2 in Cancer Therapy Resistance: From Molecular Mechanism to Future Potential

Li,

Hu,

et al. 2024

IJMS

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Tumor resistance is one of the primary reasons for cancer treatment failure, significantly limiting the options and efficacy of cancer therapies. Therefore, overcoming resistance has become a critical factor in improving cancer treatment outcomes. IGF2BP2, as a reader of m6A methylation, plays a pivotal role in the post-transcriptional regulation of RNA through the methylation of m6A sites. It not only contributes to cancer initiation and progression but also plays a key role in tumor drug resistance. This review provides a comprehensive summary of the mechanisms by which IGF2BP2 contributes to therapy resistance, with the aim of improving the efficacy of chemotherapy in cancer treatment. Advancing research in this area is crucial for developing more effective therapies that could significantly improve the quality of life for cancer patients.

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Zika virus remodels and hijacks IGF2BP2 ribonucleoprotein complex to promote viral replication organelle biogenesis

Mazeaud,

Pfister,

Owen

et al. 2024

eLife

View full text Add to dashboard Cite

Zika virus (ZIKV) infection causes significant human disease that, with no approved treatment or vaccine, constitutes a major public health concern. Its life cycle entirely relies on the cytoplasmic fate of the viral RNA genome (vRNA) through a fine-tuned equilibrium between vRNA translation, replication and packaging into new virions, all within virus-induced replication organelles (vRO). In this study, with an RNAi mini-screening and subsequent functional characterization, we have identified insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) as a new host dependency factor that regulates vRNA synthesis. In infected cells, IGF2BP2 associates with viral NS5 polymerase and redistributes to the perinuclear viral replication compartment. Combined fluorescence in situ hybridization-based confocal imaging, in vitro binding assays, and immunoprecipitation coupled to RT-qPCR, showed that IGF2BP2 directly interacts with ZIKV vRNA 3’-nontranslated region. Using ZIKV sub-genomic replicons and a replication-independent vRO induction system, we demonstrated that IGF2BP2 knockdown impairs de novo viral organelle biogenesis and, consistently, vRNA synthesis. Finally, the analysis of immunopurified IGF2BP2 complex using quantitative mass spectrometry and RT-qPCR, revealed that ZIKV infection alters the protein and RNA interactomes of IGF2BP2. Altogether, our data support that ZIKV hijacks and remodels the IGF2BP2 ribonucleoprotein complex to regulate vRO biogenesis and vRNA neosynthesis.

show abstract

The IGF2BP2-lncRNA TRPC7-AS1 axis promotes hepatocellular carcinoma cell proliferation and invasion

Cited by 5 publications

References 33 publications

Zika virus remodels and hijacks IGF2BP2 ribonucleoprotein complex to promote viral replication organelle biogenesis

Zika virus remodels and hijacks IGF2BP2 ribonucleoprotein complex to promote viral replication organelle biogenesis

The Emerging Role of IGF2BP2 in Cancer Therapy Resistance: From Molecular Mechanism to Future Potential

Zika virus remodels and hijacks IGF2BP2 ribonucleoprotein complex to promote viral replication organelle biogenesis

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