ArticleCancer research2013
Critical tumor suppressor function mediated by epithelial Mig-6 in endometrial cancer.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- MIG-6 Regulates HDAC1-Mediated Angiogenesis and Tumorigenesis in PTEN-Deficient Endometrioid Endometrial Cancer.Molecular cancer research : MCR · 2026Article
- Metformin sensitizes endometriosis to medroxyprogesterone acetate treatment through MIG-6 mediated signaling.Journal of molecular medicine (Berlin, Germany) · 2026Article
- High MIG-6 expression promotes tumor proliferation and metastasis of gastric cancer.Journal of Cancer · 2025Article
- ARG1 Is a Potential Prognostic Marker in Metastatic Endometrial Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Endometrial hyperplasia with loss of APC in a novel population of Lyz2-expressing mouse endometrial epithelial cells.Carcinogenesis · 2023Article
- MIG-6 Is Critical for Progesterone Responsiveness in Human Complex Atypical Hyperplasia and Early-Stage Endometrial Cancer.International journal of molecular sciences · 2022Article
- Mig-6 Inhibits Autophagy in HCC Cell Lines by Modulating miR-193a-3p.International journal of medical sciences · 2022Article
- Gene 33/Mig6/ERRFI1, an Adapter Protein with Complex Functions in Cell Biology and Human Diseases.Cells · 2021Review
- Long noncoding RNA ANRIL promotes the malignant progression of cholangiocarcinoma by epigenetically repressing ERRFI1 expression.Cancer science · 2020Article
- A calcium-dependent phospholipase A2 (cPLA2) expression is regulated by MIG-6 during endometrial tumorigenesis.Biochemical and biophysical research communications · 2019Article
- MIG-6 suppresses endometrial epithelial cell proliferation by inhibiting phospho-AKT.BMC cancer · 2018Article
- Article
- Panobinostat Enhances Growth Suppressive Effects of Progestin on Endometrial Carcinoma by Increasing Progesterone Receptor and Mitogen-Inducible Gene-6.Hormones & cancer · 2017Article
- LKB1 loss promotes endometrial cancer progression via CCL2-dependent macrophage recruitment.The Journal of clinical investigation · 2015Article
- Upregulation of mitogen-inducible gene 6 triggers antitumor effect and attenuates progesterone resistance in endometrial carcinoma cells.Cancer gene therapy · 2015Article
- ARID1A Is Essential for Endometrial Function during Early Pregnancy.PLoS genetics · 2015Article
- Mig-6 regulates endometrial genes involved in cell cycle and progesterone signaling.Biochemical and biophysical research communications · 2015Article
- Mig-6 suppresses endometrial cancer associated with Pten deficiency and ERK activation.Cancer research · 2014Article
- Disturbed cartilage and joint homeostasis resulting from a loss of mitogen-inducible gene 6 in a mouse model of joint dysfunction.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Mig-6 gene knockout induces neointimal hyperplasia in the vascular smooth muscle cell.Disease markers · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Endometrial cancer is preceded by endometrial hyperplasia, unopposed estrogen exposure, and genetic alterations, but the precise causes of endometrial cancer remain uncertain. Mig-6, mainly known as a negative regulator of the EGF receptor, is an important mediator of progesterone signaling in the uterus, where it mediates tumor suppression by modulating endometrial stromal-epithelial communications. In this study, we investigated the function of Mig-6 in the uterine epithelium using a tissue-specific gene knockout strategy, in which floxed Mig-6 (Mig-6(f/f)) mice were crossed to Wnt7a-Cre mice (Wnt7a(cre+)Mig-6(f/f)). Wnt7a(cre+)Mig-6(f/f) mice developed endometrial hyperplasia and estrogen-dependent endometrial cancer, exhibiting increased proliferation in epithelial cells as well as apoptosis in subepithelial stromal cells. We documented increased expression of NOTCH1 and BIRC3 in epithelial cells of Wnt7a(cre+)Mig-6(f/f) mice and decreased expression of the progesterone receptor (PR) in stromal cells. Progesterone therapy controls endometrial growth and prevents endometrial cancer, but the effectiveness of progesterone as a treatment for women with endometrial cancer is less clear. We noted that the hyperplasic phenotype of Wnt7a(cre+)Mig-6(f/f) mice was prevented by progesterone treatment, whereas this treatment had no effect in PR(cre/+)Mig-6(f/f) mice where Mig-6 was deleted in both the epithelial and stromal compartments of the uterus. In contrast, activation of progesterone signaling in the stroma regulated proliferation and apoptosis in the epithelium via suppression of ERα signaling. In summary, our results establish that epithelial Mig-6 functions as a critical tumor suppressor that mediates the ability of progesterone to prevent the development of endometrial cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.