ArticleCancer biology & therapy2019
IR-A/IGF-1R-mediated signals promote epithelial-mesenchymal transition of endometrial carcinoma cells by activating PI3K/AKT and ERK pathways.
Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Pooled it
- Targeting iNAMPT and NAD Biosynthesis to Break the Obesity-Associated Liver Cancer Link.Biomedicines · 2025Article
- Identifying antisense oligonucleotides for targeted inhibition of insulin receptor isoform A.Frontiers in oncology · 2025Article
- Etiological relationship between lipid metabolism and endometrial carcinoma.Lipids in health and disease · 2023Review
- Impact of metabolic syndrome on the risk of endometrial cancer and the role of lifestyle in prevention.Bosnian journal of basic medical sciences · 2022Review
- Intersections of endocrine pathways and the epithelial mesenchymal transition in endometrial cancer.Frontiers in oncology · 2022Review
- M2‑like tumour‑associated macrophage‑secreted IGF promotes thyroid cancer stemness and metastasis by activating the PI3K/AKT/mTOR pathway.Molecular medicine reports · 2021Article
- Insulin-Like Growth Factor 2 As a Possible Neuroprotective Agent and Memory Enhancer-Its Comparative Expression, Processing and Signaling in Mammalian CNS.International journal of molecular sciences · 2021Review
- Review
- The Role of Metabolic Syndrome in Endometrial Cancer: A Review.Frontiers in oncology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObesity is a risk factor for endometrial cancer (EC). However, it is not known how insulin receptor isoform A (IR-A) and insulin-like growth factor 1 receptor (IGF-1R), cognate receptors for insulin and IGFs, respectively, regulate malignant behaviors of EC. In this study, we examined the biological effects of IR-A/IGF-1R, explored the downstream signaling cascades, and assessed the therapeutic potential of targeting IR-A/IGF-1R in vivo.
methodsThe expression levels of IR-A and IGF-1R were examined by qRT-PCR and Western blotting. Upon down-regulating IR-A and/or IGF-1R by sh-IR-A and/or sh-IGF-1R, respectively, cell migration, invasion, apoptosis, and epithelial-mesenchymal transition (EMT) were examined by wound healing, transwell invasion, flow cytometry, and Western blotting, respectively. Furthermore, the effect of sh-IR-A and/or sh-IGF-1R on phosphatidylinositide 3-kinases (PI3K)/AKT and ERK pathways was measured by Western blotting. Lastly, we monitored xenograft growth and EMT in vivo.
resultsBoth IR-A and IGF-1R were significantly up-regulated in EC cells. Knockdown of IR-A or IGF-1R alone was sufficient to reduce migration and invasion, enhance apoptosis, and inhibit EMT of EC cells, and the most significant alterations were observed in cells co-transfected with sh-IR-A+ sh-IGF-1R. These phenotypes were associated with inactivating PI3K/AKT and ERK signaling by sh-IR-A and/or sh-IGF-1R. Consistent with in vitro findings, sh-IR-A or sh-IGF-1R significantly inhibited xenograft growth and EMT in vivo.
conclusionIR-A and IGF-1R-mediated signals, by activating PI3K/AKT and ERK pathways, can induce multiple malignant phenotypes of EC cells. Therefore, targeting IR-A or IGF-1R may provide therapeutic benefits for EC.
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