ArticleProceedings of the National Academy of Sciences of the United States of America2009
IGFBP2 is a candidate biomarker for Ink4a-Arf status and a therapeutic target for high-grade gliomas.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 61 citations in OpenAlex.
- Rodent models of tumours of the central nervous system.Molecular oncology · 2024Review
- Article
- Spatial transcriptomics analysis identifies therapeutic targets in diffuse high-grade gliomas.Frontiers in molecular neuroscience · 2024Article
- MrGPS: an m6A-related gene pair signature to predict the prognosis and immunological impact of glioma patients.Briefings in bioinformatics · 2023Article
- IGFBP2 drives epithelial-mesenchymal transition in hepatocellular carcinoma via activating the Wnt/β-catenin pathway.Infectious agents and cancer · 2023Article
- N6-methyladenosine-modified HOTAIRM1 promotes vasculogenic mimicry formation in glioma.Cancer science · 2023Article
- The cuproptosis-related signature associated with the tumor environment and prognosis of patients with glioma.Frontiers in immunology · 2022Article
- IGFBP2 promotes tumor progression by inducing alternative polarization of macrophages in pancreatic ductal adenocarcinoma through the STAT3 pathway.Cancer letters · 2021Article
- Prognostic significance of age related genes in patients with lower grade glioma.Journal of Cancer · 2020Article
- IGFBP-2 acts as a tumour suppressor and plays a role in determining chemosensitivity in bladder cancer cells.Oncotarget · 2019Article
- Expanding the scope of candidate prognostic marker IGFBP2 in glioblastoma.Bioscience reports · 2019Article
- Downregulation of CD147 induces malignant melanoma cell apoptosis via the regulation of IGFBP2 expression.International journal of oncology · 2018Article
- IDH1Oncotarget · 2018Article
- IGFBP2 expression predicts IDH-mutant glioma patient survival.Oncotarget · 2017Article
- Article
- IGFBP2 Activates the NF-κB Pathway to Drive Epithelial-Mesenchymal Transition and Invasive Character in Pancreatic Ductal Adenocarcinoma.Cancer research · 2016Article
- Glioma progression is mediated by an addiction to aberrant IGFBP2 expression and can be blocked using anti-IGFBP2 strategies.The Journal of pathology · 2016Article
- IGF-binding protein 2 is a candidate target of therapeutic potential in cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- IGFBP-2 - taking the lead in growth, metabolism and cancer.Journal of cell communication and signaling · 2015Article
- Novel anti IGFBP2 single chain variable fragment inhibits glioma cell migration and invasion.Journal of neuro-oncology · 2015Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The levels of insulin-like growth factor-binding protein 2 (IGFBP2) are elevated during progression of many human cancers. By using a glial-specific transgenic mouse system (RCAS/Ntv-a), we reported previously that IGFBP2 is an oncogenic factor for glioma progression in combination with platelet-derived growth factor-beta (PDGFB). Because the INK4a-ARF locus is often deleted in high-grade gliomas (anaplastic oligodendroglioma and glioblastoma), we investigated the effect of the Ink4a-Arf-null background on IGFBP2-mediated progression of PDGFB-initiated oligodendroglioma. We demonstrate here that homozygous deletion of Ink4a-Arf bypasses the requirement of exogenously introduced IGFBP2 for glioma progression. Instead, absence of Ink4a-Arf resulted in elevated endogenous tumor cell IGFBP2. An inverse relationship between p16(INK4a) and IGFBP2 expression was also observed in human glioma tissue samples and in 90 different cancer cell lines by using Western blotting and reverse-phase protein lysate arrays. When endogenous IGFBP2 expression was attenuated by an RCAS vector expressing antisense IGFBP2 in our mouse model, a decreased incidence of anaplastic oligodendroglioma as well as prolonged survival was observed. Thus, p16(INK4a) is a negative regulator of the IGFBP2 oncogene. Loss of Ink4a-Arf results in increased IGFBP2, which contributes to glioma progression, thereby implicating IGFBP2 as a marker and potential therapeutic target for Ink4a-Arf-deleted gliomas.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.