ArticleExperimental and therapeutic medicine2018
Insulin-like growth factor 1/insulin-like growth factor 1 receptor signaling protects against cell apoptosis through the PI3K/AKT pathway in glioblastoma cells.
Article in Experimental and therapeutic medicine, 2018. 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, 50 citations in OpenAlex.
- Redundancy in Growth Factor Receptor Signaling in Adult Astrocytoma Resistance to Small-Molecule Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2026Review
- Revealing propionate metabolism-related genes in glioblastoma and investigating their underlying mechanisms.Frontiers in oncology · 2025Article
- Review
- Interleukin 6 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- Casting Light on the Janus-Faced HMG-CoA Reductase Degradation Protein 1: A Comprehensive Review of Its Dualistic Impact on Apoptosis in Various Diseases.Molecular neurobiology · 2024Review
- In vitro culture alters cell lineage composition and cellular metabolism of bovine blastocyst†.Biology of reproduction · 2024Article
- Mechanisms Underlying the Rarity of Skeletal Muscle Cancers.International journal of molecular sciences · 2024Review
- Structural Models for a Series of Allosteric Inhibitors of IGF1R Kinase.International journal of molecular sciences · 2024Article
- Structural Models for a Series of Allosteric Inhibitors of IGF1R Kinase.bioRxiv : the preprint server for biology · 2024Article
- FOXP1 regulates the development of excitatory synaptic inputs onto striatal neurons and induces phenotypic reversal with reinstatement.Science advances · 2024Article
- Insulin and IGF-1 have both overlapping and distinct effects on CD4Scientific reports · 2024Article
- Folic Acid and Folinic Acid Protect Hearts of Aging Triple-transgenic Alzheimer's Disease mice via IGF1R/PI3K/AKT and SIRT1/AMPK Pathways.Neurotoxicity research · 2023Article
- Transcriptome alterations in peripheral blood B cells of patients with multiple sclerosis receiving immune reconstitution therapy.Journal of neuroinflammation · 2023Article
- Pilot dose-ranging of rhIGF-1/rhIGFBP-3 in a preterm lamb model of evolving bronchopulmonary dysplasia.Pediatric research · 2023Article
- Advancements, Challenges, and Future Directions in Tackling Glioblastoma Resistance to Small Kinase Inhibitors.Cancers · 2022Review
- Eupalinolide O Induces Apoptosis in Human Triple-Negative Breast Cancer Cells via Modulating ROS Generation and Akt/p38 MAPK Signaling Pathway.Journal of oncology · 2022Article
- Knockdown of miR-372-3p Inhibits the Development of Diabetic Cardiomyopathy by Accelerating Angiogenesis via Activating the PI3K/AKT/mTOR/HIF-1Oxidative medicine and cellular longevity · 2022Article
- ADSC-Based Cell Therapies for Musculoskeletal Disorders: A Review of Recent Clinical Trials.International journal of molecular sciences · 2021Review
- Viruses and Metabolism: The Effects of Viral Infections and Viral Insulins on Host Metabolism.Annual review of virology · 2021Review
- RFX1: a promising therapeutic arsenal against cancer.Cancer cell international · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is a malignant tumor caused by complex pathological mechanisms, and is characterized by a high rate of cancer-related mortality and poor patient prognosis. Overgrowth of cancer cells, which results from the inhibition of cell apoptosis and/or the promotion of cell proliferation, leads to the progression of GBM. Therefore, studies into the regulatory mechanisms of cancer cell growth in GBM are required to identify potential therapeutic targets and improve treatment for GBM. In the present study, the role of insulin-like growth factor 1 (IGF1)/IGF1 receptor (IGF1R) signaling in the survival of GBM cells was evaluated. It was observed that IGF1 significantly inhibited the intrinsic and extrinsic pathways of apoptosis (P<0.05), and overexpression of IGF1R significantly promoted the survival of GBM cells (P<0.05). Moreover, both exogenous IGF1 and overexpression of IGF1R promoted the phosphorylation of protein kinase B (AKT), and inhibition of the phosphoinositide 3-kinase (PI3K)/AKT pathway significantly attenuated the inhibitory effects of IGF1/IGF1R on GBM apoptosis (P<0.05). Collectively, these findings indicate that IGF1/IGF1R promotes the survival of GBM cells through activation of the PI3K/AKT pathway. Therefore, inhibition of IGF1/IGF1R may be a viable therapeutic strategy to suppress the progression of GBM.
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