ArticleCancer research2014
Mig-6 suppresses endometrial cancer associated with Pten deficiency and ERK activation.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Genetic overlap between endometriosis and endometrial cancer: evidence from cross-disease genetic correlation and GWAS meta-analyses.Cancer medicine · 2018Pooled it
- Human biomarker navigator.iMeta · 2026Review
- Co-mutations of CTNNB1 and PTEN drive aggressive tumor progression in endometrial cancer.Disease models & mechanisms · 2026Article
- MIG-6 Regulates HDAC1-Mediated Angiogenesis and Tumorigenesis in PTEN-Deficient Endometrioid Endometrial Cancer.Molecular cancer research : MCR · 2026Article
- Exposure to phthalates enhances estrogen and beta-catenin signaling pathways, leading to endometrial hyperplasia in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- ob/ob obese mice promote tumorigenesis of endometrial cancer associated with Pten deficiency.Endocrine-related cancer · 2025Article
- UterineCancers · 2025Article
- Role of Mig-6 in adipose tissue: Implications for glucose metabolism and insulin resistance.PloS one · 2025Article
- Research Advances in Adenomyosis-Related Signaling Pathways and Promising Targets.Biomolecules · 2024Review
- ERBB2 Targeting Reveals a Significant Suppression of Tumorigenesis in Murine Endometrial Cancer with Pten Mutation.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- ARG1 Is a Potential Prognostic Marker in Metastatic Endometrial Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Development of adverse outcome pathways relevant for the identification of substances having endocrine disruption properties Uterine adenocarcinoma as adverse outcome.EFSA journal. European Food Safety Authority · 2023Article
- MIG-6 Is Critical for Progesterone Responsiveness in Human Complex Atypical Hyperplasia and Early-Stage Endometrial Cancer.International journal of molecular sciences · 2022Article
- Gene 33/Mig6/ERRFI1, an Adapter Protein with Complex Functions in Cell Biology and Human Diseases.Cells · 2021Review
- ARID1A and PGR proteins interact in the endometrium and reveal a positive correlation in endometriosis.Biochemical and biophysical research communications · 2021Article
- PADI2-Catalyzed MEK1 Citrullination Activates ERK1/2 and Promotes IGF2BP1-Mediated SOX2 mRNA Stability in Endometrial Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- β-catenin activates TGF-β-induced epithelial-mesenchymal transition in adenomyosis.Experimental & molecular medicine · 2020Article
- Long noncoding RNA ANRIL promotes the malignant progression of cholangiocarcinoma by epigenetically repressing ERRFI1 expression.Cancer science · 2020Article
- Overexpression of MIG-6 in the cartilage induces an osteoarthritis-like phenotype in mice.Arthritis research & therapy · 2020Article
- Unexplained recurrent pregnancy loss and unexplained infertility: twins in disguise.Human reproduction open · 2020Article
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Authors and funding
12 authors.
Funding
Abstract
PTEN mutations are the most common genetic alterations in endometrial cancer. Loss of PTEN and subsequent AKT activation stimulate estrogen receptor α-dependent pathways that play an important role in endometrial tumorigenesis. The major pathologic phenomenon of endometrial cancer is the loss of ovarian steroid hormone control over uterine epithelial cell proliferation and apoptosis. However, the precise mechanism of PTEN/AKT signaling in endometrial cancer remains poorly understood. The progesterone signaling mediator MIG-6 suppresses estrogen signaling and it has been implicated previously as a tumor suppressor in endometrial cancer. In this study, we show that MIG-6 also acts as a tumor suppressor in endometrial cancers associated with PTEN deficiency. Transgenic mice, where Mig-6 was overexpressed in progesterone receptor-expressing cells, exhibited a relative reduction in uterine tumorigenesis caused by Pten deficiency. ERK1/2 was phosphorylated in uterine tumors and administration of an ERK1/2 inhibitor suppressed cancer progression in PR(cre/+)Pten(f/f) mice. In clinical specimens of endometrial cancer, MIG-6 expression correlated inversely with ERK1/2 phosphorylation during progression. Taken together, our findings suggest that Mig-6 regulates ERK1/2 phosphorylation and that it is crucial for progression of PTEN-mutant endometrial cancers, providing a mechanistic rationale for the evaluation of ERK1/2 inhibitors as a therapeutic treatment in human endometrial cancer.
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