ArticleOncotarget2017
miR-29a regulated ER-positive breast cancer cell growth and invasion and is involved in the insulin signaling pathway.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- Insulin Resistance: The Increased Risk of Cancers.Current oncology (Toronto, Ont.) · 2024Review
- Metformin counteracts stimulatory effects induced by insulin in primary breast cancer cells.Journal of translational medicine · 2022Article
- Therapeutic potential of anti-miR29a in breast cancer patients with type 2 diabetes: anTranslational cancer research · 2022Article
- Decoding Insulin-Like Growth Factor Signaling Pathway From a Non-coding RNAs Perspective: A Step Towards Precision Oncology in Breast Cancer.Journal of mammary gland biology and neoplasia · 2022Review
- CASP9 As a Prognostic Biomarker and Promising Drug Target Plays a Pivotal Role in Inflammatory Breast Cancer.International journal of analytical chemistry · 2022Article
- Radiation increases COL1A1, COL3A1, and COL1A2 expression in breast cancer.Open medicine (Warsaw, Poland) · 2022Article
- Identification of a six-microRNA signature as a potential diagnostic biomarker in breast cancer tissues.Journal of clinical laboratory analysis · 2021Article
- Article
- A microRNA-clinical prognosis model to predict the overall survival for kidney renal clear cell carcinoma.Cancer medicine · 2021Article
- MicroRNA in combination with HER2-targeting drugs reduces breast cancer cell viability in vitro.Scientific reports · 2021Article
- Serum miR-29a/b expression in gestational diabetes mellitus and its influence on prognosis evaluation.The Journal of international medical research · 2020Article
- Global targetome analysis reveals critical role of miR-29a in pancreatic stellate cell mediated regulation of PDAC tumor microenvironment.BMC cancer · 2020Article
- Article
- Cdc42: A Novel Regulator of Insulin Secretion and Diabetes-Associated Diseases.International journal of molecular sciences · 2019Review
- miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42/International journal of endocrinology · 2019Article
- Anticancer effect of HOTTIP regulates human pancreatic cancer via the metabotropic glutamate receptor 1 pathway.Oncology letters · 2018Article
- Glycans as Regulatory Elements of the Insulin/IGF System: Impact in Cancer Progression.International journal of molecular sciences · 2017Review
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
Increasing amounts of evidence show that insulin can activate different insulin signaling pathways to promote breast cancer growth and invasion. miR-29a plays crucial roles in decreasing glucose-stimulated insulin secretion, as well as in regulating breast cancer cell proliferation and EMT. However, the mechanism responsible for the regulatory effects of miR-29a on breast cancer growth and invasion and the relationship between these effects and insulin signaling remains unclear. Herein, we showed that human insulin increased miR-29a expression in ER-positive breast cancer cells and that miR-29a facilitated the ability of insulin to promote breast cancer cell proliferation and migration. We found that miR-29a-induced cell proliferation and metastasis acceleration occurred primarily through ERK phosphorylation. The IGF-1R is the upstream target gene of miR-29a, while CDC42 and p85α are the downstream target genes of miR-29a. These results have provided us with information regarding the molecular mechanisms by which hyperinsulinemia promotes breast cancer occurrence and development and thus leads to a poor prognosis in breast cancer patients and indicate that miR-29a plays an important role in breast cancer development and invasion.
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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.