ArticleJournal of cellular and molecular medicine2019
Targeting EZH2 as a novel therapeutic strategy for sorafenib-resistant thyroid carcinoma.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Therapeutic Potential of Tyrosine Kinase Inhibitors in Advanced Thyroid Cancer.Current oncology reports · 2026Review
- Review
- A Cuproptosis-Related gene Signature as a Prognostic Biomarker in Thyroid Cancer Based on Transcriptomics.Biochemical genetics · 2025Article
- MicroRNA-mediated autophagy regulation in thyroid cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Therapeutic potential of microRNA-506 in cancer treatment: mechanisms and therapeutic implications.Frontiers in oncology · 2025Review
- Advances in the molecular mechanism and targeted therapy of radioactive-iodine refractory differentiated thyroid cancer.Medical oncology (Northwood, London, England) · 2023Review
- Crosstalk between Noncoding RNAs and the Epigenetics Machinery in Pediatric Tumors and Their Microenvironment.Cancers · 2023Review
- Epigenetic Targets and Their Inhibitors in Thyroid Cancer Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Molecular mechanisms of resistance to kinase inhibitors and redifferentiation in thyroid cancers.Endocrine-related cancer · 2022Review
- Pyruvate carboxylase promotes malignant transformation of papillary thyroid carcinoma and reduces iodine uptake.Cell death discovery · 2022Article
- Protein tyrosine kinase inhibitor resistance in malignant tumors: molecular mechanisms and future perspective.Signal transduction and targeted therapy · 2022Review
- Histone Modifications and Non-Coding RNAs: Mutual Epigenetic Regulation and Role in Pathogenesis.International journal of molecular sciences · 2022Review
- State of the Art in the Current Management and Future Directions of Targeted Therapy for Differentiated Thyroid Cancer.International journal of molecular sciences · 2022Review
- A metabolism-related gene signature for predicting the prognosis in thyroid carcinoma.Frontiers in genetics · 2022Article
- Histone H3 lysine-trimethylation markers are decreased by recombinant methioninase and increased by methotrexate at concentrations which inhibit methionine-addicted osteosarcoma cell proliferation.Biochemistry and biophysics reports · 2021Article
- The potential role of miR-124-3p in tumorigenesis and other related diseases.Molecular biology reports · 2021Review
- Effects of Sorafenib, a Tyrosin Kinase Inhibitor, on Adrenocortical Cancer.Frontiers in endocrinology · 2021Article
- KCNQ1OT1 contributes to sorafenib resistance and programmed death‑ligand‑1‑mediated immune escape via sponging miR‑506 in hepatocellular carcinoma cells.International journal of molecular medicine · 2020Article
- ncDRMarker: a computational method for identifying non-coding RNA signatures of drug resistance based on heterogeneous network.Annals of translational medicine · 2020Article
- Combined tazemetostat and MAPKi enhances differentiation of papillary thyroid cancer cells harbouring BRAFJournal of cellular and molecular medicine · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid carcinoma is the most common endocrine malignancy. Surgery, post-operative selective iodine-131 and thyroid hormone suppression were the most common methods for the therapy of thyroid carcinoma. Although most patients with differentiated thyroid carcinoma (DTC) showed positive response for these therapeutic methods, some patients still have to face the radioactive iodine (RAI)-refractory problems. Sorafenib is an oral multikinase inhibitor for patients with advanced RAI refractory DTC. However, the side effects and drug resistance of sorafenib suggest us to develop novel drugs and strategies for the therapy of thyroid carcinoma. In this study, we firstly found that patients with sorafenib resistance showed no significant change in rapidly accelerated fibrosarcoma and VEGFR expression levels compared with sorafenib sensitive patients. Moreover, a further miRNAs screen by qRT-PCR indicated that miR-124-3p and miR-506-3p (miR-124/506) were remarkably reduced in sorafenib insensitive patients. With a bioinformatics prediction and functional assay validation, we revealed that enhancer of zeste homolog 2 (EZH2) was the direct target for miR-124/506. Interestingly, we finally proved that the sorafenib resistant cells regained sensitivity for sorafenib by EZH2 intervention with miR-124/506 overexpression or EZH2 inhibitor treatment in vitro and in vivo, which will lead to the decreased tri-methylation at lysine 27 of histone H3 (H3K27me3) and increased acetylated lysine 27 of histone H3 (H3K27ac) levels. Therefore, we conclude that the suppression of EZH2 represents a potential target for thyroid carcinoma therapy.
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