ArticleBMC cancer2020
Suppression of Mig-6 overcomes the acquired EGFR-TKI resistance of lung adenocarcinoma.
Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Reduced circulating Mig-6 levels are associated with dysglycemia in metabolic dysfunction associated steatotic liver disease (MASLD).BMJ open diabetes research & care · 2026Article
- The neural crest-associated gene ERRFI1 is involved in melanoma progression and resistance toward targeted therapy.Molecular oncology · 2026Article
- Functional loss of ERBB receptor feedback inhibitor 1 (MIG6) promotes glioblastoma tumorigenesis by aberrant activation of epidermal growth factor receptor (EGFR).Molecular oncology · 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
- MIG6 loss confers resistance to ALK/ROS1 inhibitors in NSCLC through EGFR activation by low-dose EGF.JCI insight · 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
- ADCY9 functions as a novel cancer suppressor gene in lung adenocarcinoma.Journal of thoracic disease · 2023Article
- Cosuppression of NF-κB and AICDA Overcomes Acquired EGFR-TKI Resistance in Non-Small Cell Lung Cancer.Cancers · 2022Article
- Gene 33/Mig6/ERRFI1, an Adapter Protein with Complex Functions in Cell Biology and Human Diseases.Cells · 2021Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe resistance of lung cancer to epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is one of the unconquered frontiers in chemotherapy. Mitogen-inducible gene 6 (Mig-6) is known to inhibit the kinase activity of epidermal growth factor receptor (EGFR). Similarly, numerous studies of mouse models suggested tumor suppressive function of Mig-6 in lung cancer. On the contrary, the results of clinical investigations revealed that lung cancer patients with elevated expression of Mig-6 are associated with a poor prognosis. More recent work showed that unlike wild type (WT) EGFR, mutant EGFR phosphorylates Mig-6 and phosphorylated Mig-6 negatively regulates the degradation of EGFR mutants in lung adenocarcinoma. Here, we tried to untangle the controversies surrounding Mig-6 function as a protagonist or an antagonist of EGFR-TKI resistant lung cancer.
methodsWe compared the expression and phosphorylation status of Mig-6 in the EGFR-TKI resistant lung adenocarcinoma (PC9/GR cells) to EGFR-TKI sensitive lung adenocarcinoma (PC9 cells). We investigated the function of Mig-6 by either depletion or overexpression of Mig-6 in those cells and evaluated the efficacy of combining of Mig-6 knock-down and EGFR-TKI treatment in PC9/GR. The correlation between Mig-6 expressions and the prognoses of lung adenocarcinoma was examined by The Cancer Genome Atlas (TCGA) data and clinical samples.
resultsOur results indicated that the expression of Mig-6 was significantly increased in PC9/GR cells compared to that of PC9 cells. The significant portion of Mig-6 existed as a phosphorylated form in PC9 and PC9/GR cells. Moreover, overexpression of Mig-6 significantly increased the cell proliferation, invasion and epithelial mesenchymal transition (EMT) in PC9 cells. Combination of Mig-6 knock-down and EGFR-TKI treatment significantly overcame the EGFR-TKI resistance of PC9/GR cells. In addition, our analyses of clinical samples confirmed that high Mig-6 expressions positively correlate with a poor prognosis and EGFR-TKI resistance in lung adenocarcinoma.
conclusionOur findings reinforce scientific notion of Mig-6 as an oncoprotein in the context of EGFR-TKI resistant lung adenocarcinoma. We propose that targeting Mig-6 may be a promising strategy to overcome the EGFR-TKI resistance in lung cancer.
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