ArticleJournal of cell communication and signaling2015
Involvement of the insulin-like growth factor binding proteins in the cancer cell response to DNA damage.
Article in Journal of cell communication and signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- The mechanism of high mobility group box-1 in the proliferation and macrophage polarization in esophageal squamous cell carcinoma cells.European journal of medical research · 2025Article
- Identification of 10 differentially expressed genes involved in the tumorigenesis of cervical cancerPeerJ · 2024Article
- Signaling Pathways of the Insulin-like Growth Factor Binding Proteins.Endocrine reviews · 2023Article
- Genome-wide analyses characterize shared heritability among cancers and identify novel cancer susceptibility regions.Journal of the National Cancer Institute · 2023Article
- The Integrative Studies on the Functional A-to-I RNA Editing Events in Human Cancers.Genomics, proteomics & bioinformatics · 2023Article
- Expression characteristics and their functional role of IGFBP gene family in pan-cancer.BMC cancer · 2023Article
- Comparison of Proteomic Expression Profiles after Radiation Exposure across Four Different Species.Radiation research · 2022Article
- IGFBP-3 functions as a molecular switch that mediates mitochondrial and metabolic homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Insulin-like growth factors: Ligands, binding proteins, and receptors.Molecular metabolism · 2021Review
- KIF15 is involved in development and progression of Burkitt lymphoma.Cancer cell international · 2021Article
- Insulin-Like Growth Factor Binding Protein-3 Binds to Histone 3.International journal of molecular sciences · 2021Article
- The Mutant p53-Driven Secretome Has Oncogenic Functions in Pancreatic Ductal Adenocarcinoma Cells.Biomolecules · 2020Article
- Glucose-dependent GPER1 expression modulates tamoxifen-induced IGFBP-1 accumulation.Journal of molecular endocrinology · 2019Article
- Chrysin Increases the Therapeutic Efficacy of Docetaxel and Mitigates Docetaxel-Induced Edema.Integrative cancer therapies · 2017Article
- DNA damage response and sphingolipid signaling in liver diseases.Surgery today · 2016Review
- Involvement of p53 in insulin-like growth factor binding protein-3 regulation in the breast cancer cell response to DNA damage.Oncotarget · 2015Article
- Serum Proteins as New Biomarkers for Whole-Body Exposure to High- and Low-LET Ionizing Radiation.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complex mechanisms that cells have evolved to meet the challenge of constant exposure to DNA-damaging stimuli, also serve to protect cancer cells from the cytotoxic effects of chemo- and radiotherapy. IGFBPs appear to be involved, directly or indirectly, in some of these protective mechanisms. Activation of p53 is an early response to genotoxic stress, and all six human IGFBP genes have predicted p53 response elements in their promoter and/or intronic regions, at least some of which are functional. IGFBP3 has been extensively characterized as a p53-inducible gene, but in some cases it is suppressed by mutant p53 forms. DNA double-strand breaks (DSBs), induced by radiotherapy and some chemotherapies, potentially lead to apoptotic cell death, senescence, or repair and recovery. DSB damage can be repaired by homologous recombination or non-homologous end-joining (NHEJ), depending on the cell cycle stage, availability of key repair proteins, and other factors. The epidermal growth factor receptor (EGFR) has been implicated in the NHEJ pathway, and EGFR inhibition may inhibit repair, promoting apoptosis and thus improving sensitivity to chemotherapy or radiotherapy. Both IGFBP-3 and IGFBP-6 interact with components of the NHEJ pathway, and IGFBP-3 can facilitate this process through direct interaction with both EGFR and the catalytic subunit of DNA-PK. Cell fate after DNA damage may in part be regulated by the balance between the sphingolipids ceramide and sphingosine-1-phosphate, and IGFBPs can influence the production of both lipids. A better understanding of the involvement of IGFBPs in the DNA damage response in cancer cells may lead to improved methods of sensitizing cancers to DNA-damaging therapies.
Identifiers
What OpenQuestion holds
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.