ArticleMediators of inflammation2019
IGF-1R Inhibition Suppresses Cell Proliferation and Increases Radiosensitivity in Nasopharyngeal Carcinoma Cells.
Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Loss of IGF-1R impairs DNA-PKcs recruitment to chromatin leading to defective end-joining.Molecular oncology · 2026Article
- Article
- Prognostic value of FLOT1-related gene signature in head and neck squamous cell carcinoma: insights into radioresistance mechanisms and clinical outcomes.Cell death discovery · 2025Article
- MAZ-mediated tumor progression and immune evasion in hormone receptor-positive breast cancer: Targeting tumor microenvironment and PCLAF+ subtype-specific therapy.Translational oncology · 2025Article
- Assessing insulin resistance: the triglyceride-glucose index as a predictor of survival in nasopharyngeal carcinoma.Frontiers in physiology · 2025Article
- Circ_0006174 Upregulates IGF1R to Enhance Radioresistance and Tumorigenesis in Colorectal Cancer via miR-940 Suppression.Applied biochemistry and biotechnology · 2025Article
- Advances in research on RNA methylation and cancer radiotherapy resistance.Frontiers in oncology · 2025Review
- IGF-1R mediates crosstalk between nasopharyngeal carcinoma cells and osteoclasts and promotes tumor bone metastasis.Journal of experimental & clinical cancer research : CR · 2024Article
- A preclinical model of patient-derived cerebrospinal fluid circulating tumor cells for experimental therapeutics in leptomeningeal disease from melanoma.Neuro-oncology · 2022Article
- Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma.Molecular medicine reports · 2021Article
- Novel Regulators of the IGF System in Cancer.Biomolecules · 2021Review
- Radiation induces epithelial to mesenchymal transition via upregulation of PD-L1 in nasopharyngeal carcinoma cell.Translational cancer research · 2021Article
- Silencing circPVT1 enhances radiosensitivity in non-small cell lung cancer by sponging microRNA-1208.Cancer biomarkers : section A of Disease markers · 2021Article
- Upregulating the Expression of LncRNA ANRIL Promotes Osteogenesis via the miR-7-5p/IGF-1R Axis in the Inflamed Periodontal Ligament Stem Cells.Frontiers in cell and developmental biology · 2021Article
- The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia.Frontiers in cell and developmental biology · 2021Review
- Depletion of insulin-like growth factor 1 receptor increases radiosensitivity in colorectal cancer.Journal of gastrointestinal oncology · 2020Article
- Design, Synthesis, and Biological Evaluation of Proteolysis Targeting Chimeras (PROTACs) for the Dual Degradation of IGF-1R and Src.Molecules (Basel, Switzerland) · 2020Article
- FOXD1, negatively regulated by miR-186, promotes the proliferation, metastasis and radioresistance of nasopharyngeal carcinoma cells.Cancer biomarkers : section A of Disease markers · 2020Observational
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Authors and funding
10 authors.
Funding
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Abstract
Although ionizing radiation (IR) has provided considerable improvements in nasopharyngeal carcinoma (NPC) treatment, radioresistance is still a major threat for some subsets of patients. The insulin-like growth factor-1 receptor (IGF-1R) signaling pathway is tightly regulated and plays critical roles in mediating cell proliferation, growth, and survival. Thus, IGF-1R may be a potential therapeutic target for patients with different malignancies. However, its mechanism in NPC is not fully investigated. Linsitinib is an oral small molecule and is a tyrosine kinase inhibitor (TKI) of IGF-1R, which has been known for antitumor effects used widely. Here, we evaluated the proliferation and radiosensitivity of NPC cell lines (CNE-2 and SUNE-1) after linsitinib treatment. We found that linsitinib suppresses IGF-1-induced cell proliferation through inhibiting Akt and ERK phosphorylation. Moreover, linsitinib further boosted IR-induced DNA damage, G2-M cell cycle delay, and apoptosis in NPC cells. Finally, linsitinib reversed radioresistant NPC cells by decreasing the phosphorylation of IGF-1R. Our data indicated that the combination of linsitinib and IR and targeting IGF-1R by linsitinib could be a promising therapeutic strategy for NPC.
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