ArticleOncotarget2015
FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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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
73 citing papers in PubMed, 122 citations in OpenAlex.
- A Phase 0 Trial of Ceritinib in Patients with Brain Metastases and Recurrent Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- Estrogen promotes tumor phenotypes in ER+ and ER- breast cancer through UGDH-GPR30.JCI insight · 2026Article
- Integrative systems biology identifies PSMB2 as a core oxidative stress-associated target in triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- TMEM216 inhibits breast cancer lung metastasis by modulating IGF1R-IRS4 signaling pathway.Nature communications · 2026Article
- Targeting EGFR/IGF-IR Functional Crosstalk in 2D and 3D Triple-Negative Breast Cancer Models to Evaluate Tumor Progression.International journal of molecular sciences · 2025Article
- Signaling pathways as the pivotal regulators of cisplatin resistance in tumor cells through SOX2 upregulation.Medical oncology (Northwood, London, England) · 2025Review
- IGF1R activates FOXP3-β-catenin signaling to promote breast cancer development.Breast cancer research and treatment · 2025Article
- Exercise-Induced Reduction of IGF1R Sumoylation Attenuates Neuroinflammation in APP/PS1 Transgenic Mice.Journal of advanced research · 2025Article
- A novel FAK-degrading PROTAC molecule exhibited both anti-tumor activities and efficient MDR reversal effects.Acta pharmacologica Sinica · 2024Article
- Article
- Role of Insulin-like Growth Factor-1 Receptor in Tobacco Smoking-Associated Lung Cancer Development.Biomedicines · 2024Review
- IGF-1R mediates crosstalk between nasopharyngeal carcinoma cells and osteoclasts and promotes tumor bone metastasis.Journal of experimental & clinical cancer research : CR · 2024Article
- Current progress and prospects for G protein-coupled estrogen receptor in triple-negative breast cancer.Frontiers in cell and developmental biology · 2024Review
- Long non-coding RNAs as the critical regulators of PI3K/AKT, TGF-β, and MAPK signaling pathways during breast tumor progression.Journal of translational medicine · 2023Review
- What role does PDL1 play in EMT changes in tumors and fibrosis?Frontiers in immunology · 2023Review
- The Insulin-like Growth Factor Signaling Pathway in Breast Cancer: An Elusive Therapeutic Target.Life (Basel, Switzerland) · 2022Review
- Article
- LMOD1, an oncogene associated with Lauren classification, regulates the metastasis of gastric cancer cells through the FAK-AKT/mTOR pathway.BMC cancer · 2022Article
- Tumor suppressive role of microRNA-4731-5p in breast cancer through reduction of PAICS-induced FAK phosphorylation.Cell death discovery · 2022Article
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Triple negative breast cancer (TNBC) is a highly metastatic disease that currently lacks effective prevention and treatment strategies. The insulin-like growth factor 1 receptor (IGF1R) and focal adhesion kinase (FAK) signaling pathways function in numerous developmental processes, and alterations in both are linked with a number of common pathological diseases. Overexpression of IGF1R and FAK are closely associated with metastatic breast tumors. The present study investigated the interrelationship between IGF1R and FAK signaling in regulating the malignant properties of TNBC cells. Using small hairpin RNA (shRNA)-mediated IGF1R silencing methods, we showed that IGF1R is essential for sustaining mesenchymal morphologies of TNBC cells and modulates the expression of EMT-related markers. We further showed that IGF1R overexpression promotes migratory and invasive behaviors of TNBC cell lines. Most importantly, IGF1R-driven migration and invasion is predominantly mediated by FAK activation and can be suppressed using pharmacological inhibitors of FAK. Our findings in TNBC cells demonstrate a novel role of the IGF1R/FAK signaling pathway in regulating critical processes involved in the metastatic cascade. These results may improve the current understanding of the basic molecular mechanisms of TNBC metastasis and provide a strong rationale for co-targeting of IGF1R and FAK as therapy for mesenchymal TNBCs.
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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.