ArticleCancer discovery2015
Loss of MIG6 Accelerates Initiation and Progression of Mutant Epidermal Growth Factor Receptor-Driven Lung Adenocarcinoma.
Article in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 75 citations in OpenAlex.
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- Functional loss of ERBB receptor feedback inhibitor 1 (MIG6) promotes glioblastoma tumorigenesis by aberrant activation of epidermal growth factor receptor (EGFR).Molecular oncology · 2025Article
- Epsin3 promotes non-small cell lung cancer progression via modulating EGFR stability.Cell & bioscience · 2025Article
- High MIG-6 expression promotes tumor proliferation and metastasis of gastric cancer.Journal of Cancer · 2025Article
- Mutations in Mig6 reduce inhibition of the epidermal growth factor receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Potentially functional variants of ERRFI1 in hypoxia-related genes predict survival of non-small cell lung cancer patients.Cancer medicine · 2024Article
- SOS2 modulates the threshold of EGFR signaling to regulate osimertinib efficacy and resistance in lung adenocarcinoma.Molecular oncology · 2024Article
- MIG6 Mediates Adaptive and Acquired Resistance to ALK/ROS1 Fusion Kinase Inhibition through EGFR Bypass Signaling.Molecular cancer therapeutics · 2024Article
- MIG6 loss confers resistance to ALK/ROS1 inhibitors in NSCLC through EGFR activation by low-dose EGF.JCI insight · 2023Article
- JMJD5 inhibits lung cancer progression by facilitating EGFR proteasomal degradation.Cell death & disease · 2023Article
- Intervention of AXL in EGFR Signaling via Phosphorylation and Stabilization of MIG6 in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2023Article
- Kremen2 drives the progression of non-small cell lung cancer by preventing SOCS3-mediated degradation of EGFR.Journal of experimental & clinical cancer research : CR · 2023Article
- JAC4 Inhibits EGFR-Driven Lung Adenocarcinoma Growth and Metastasis through CTBP1-Mediated JWA/AMPK/NEDD4L/EGFR Axis.International journal of molecular sciences · 2023Article
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17 authors at 5 institutions in 2 countries.
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Abstract
unlabelledSomatic mutations in the EGFR kinase domain drive lung adenocarcinoma. We have previously identified MIG6, an inhibitor of ERBB signaling and a potential tumor suppressor, as a target for phosphorylation by mutant EGFRs. Here, we demonstrate that MIG6 is a tumor suppressor for the initiation and progression of mutant EGFR-driven lung adenocarcinoma in mouse models. Mutant EGFR-induced lung tumor formation was accelerated in Mig6-deficient mice, even with Mig6 haploinsufficiency. We demonstrate that constitutive phosphorylation of MIG6 at Y394/Y395 in EGFR-mutant human lung adenocarcinoma cell lines is associated with an increased interaction of MIG6 with mutant EGFR, which may stabilize EGFR protein. MIG6 also fails to promote mutant EGFR degradation. We propose a model whereby increased tyrosine phosphorylation of MIG6 decreases its capacity to inhibit mutant EGFR. Nonetheless, the residual inhibition is sufficient for MIG6 to delay mutant EGFR-driven tumor initiation and progression in mouse models. SIGNIFICANCE: This study demonstrates that MIG6 is a potent tumor suppressor for mutant EGFR-driven lung tumor initiation and progression in mice and provides a possible mechanism by which mutant EGFR can partially circumvent this tumor suppressor in human lung adenocarcinoma.
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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.