ArticleOncogene2018
MicroRNA-146b promotes PI3K/AKT pathway hyperactivation and thyroid cancer progression by targeting PTEN.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 107 citations in OpenAlex.
- Recent Advances in the Treatment of Thyroid Pathologies with Selenium-Containing Compounds, Nanoparticles and Nanocomplexes Based on Selenium and Selenoproteins.Biological trace element research · 2026Review
- Primary endometrioid adenocarcinoma of the vagina after total hysterectomy for adenomyosis: A case report.Oncology letters · 2026Article
- Glucose Metabolic Reprogramming in Thyroid Cancer: Underlying Molecular Mechanisms and Links to Progression and Treatment.Current medical science · 2026Review
- Dedifferentiation and Redifferentiation of Follicular-Cell-Derived Thyroid Carcinoma: Mechanisms and Therapeutic Implications.Biomedicines · 2025Review
- Somatic genetic alterations in the development and progression in thyroid tumors of follicular cells.European thyroid journal · 2025Review
- MiR-146b overexpression promotes bladder cancer cell growth via the SMAD4/C-MYC/Cyclin D1 axis.Frontiers in oncology · 2025Article
- PTEN inhibits epithelial mesenchymal transition of thyroid cancer cells by regulating the Wnt/β-Catenin signaling pathway.Discover oncology · 2024Article
- Genomic alterations in thyroid cancer: biological and clinical insights.Nature reviews. Endocrinology · 2024Review
- The prognostic power of gene mutations in thyroid cancer.Endocrine connections · 2024Review
- Loss of RACK1 promotes glutamine addiction via activating AKT/mTOR/ASCT2 axis to facilitate tumor growth in gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- CVD phenotyping in oncologic disorders: cardio-miRNAs as a potential target to improve individual outcomes in revers cardio-oncology.Journal of translational medicine · 2024Review
- Common biological processes and mutual crosstalk mechanisms between cardiovascular disease and cancer.Frontiers in oncology · 2024Review
- The role of genetic and epigenetic modifications as potential biomarkers in the diagnosis and prognosis of thyroid cancer.Frontiers in oncology · 2024Review
- Mechanistic Insights of Thyroid Cancer Progression.Endocrinology · 2023Review
- MiR-146b-5p regulates the scavenging effect of GPx-3 on peroxide in papillary thyroid cancer cells.Heliyon · 2023Article
- CircNDST1 promotes papillary thyroid cancer progression via its interaction with CSNK2A1 to activate the PI3K-Akt pathway and epithelial-mesenchymal transition.Journal of endocrinological investigation · 2023Article
- Association of endometriosis with cardiovascular disease: Genetic aspects (Review).International journal of molecular medicine · 2023Review
- Using CRISPR/Cas9 to Edit a Thyroid Cancer Cell Line.Advances in experimental medicine and biology · 2023Article
- Dysregulation of miRISC Regulatory Network Promotes Hepatocellular Carcinoma by Targeting PI3K/Akt Signaling Pathway.International journal of molecular sciences · 2022Article
- Hsa-miR-143-3p inhibits Wnt-β-catenin and MAPK signaling in human corneal epithelial stem cells.Scientific reports · 2022Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that miR-146b is the most upregulated microRNA in thyroid cancer and has a central role in cancer progression through mechanisms that remain largely unidentified. As phosphoinositide 3-kinase/protein kinase-B (PI3K/AKT) signaling is a fundamental oncogenic driver in many thyroid cancers, we explored a potential role for miR-146b and its target genes in PI3K/AKT activation. Among the predicted target genes of miR-146b, we found the tumor-suppressor phosphatase and tensin homolog (PTEN). Constitutive overexpression of miR-146b in thyroid epithelial cell lines significantly decreased PTEN mRNA and protein levels by direct binding to its 3'-UTR. This was accompanied by PI3K/AKT hyperactivation, leading to the exclusion of FOXO1 and p27 from the nucleus and a corresponding increase in cellular proliferation. Moreover, miR-146b overexpression led to protection from apoptosis and an increased migration and invasion potential, regulating genes involved in epithelial-mesenchymal transition. Notably, with the single exception of E-cadherin expression, all of these outcomes could be reversed by PTEN coexpression. Further analysis showed that miR-146b directly inhibits E-cadherin expression through binding to its 3'-UTR. Interestingly, miR-146b inhibition in human thyroid tumor xenografts, using a synthetic and clinically amenable molecule, blocked tumor growth when delivered intratumorally. Importantly, this inhibition increased PTEN protein levels. In conclusion, our data define a novel mechanism of PI3K/AKT hyperactivation and outline a regulatory role for miR-146b in suppressing PTEN expression, a frequent observation in thyroid cancer. Both events are related to a more aggressive tumoral phenotype. Targeting miR-146b therefore represents a promising therapeutic strategy for the treatment of this disease.
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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.