ArticleThe Journal of clinical endocrinology and metabolism2017
Targeting MYC as a Therapeutic Intervention for Anaplastic Thyroid Cancer.
Article in The Journal of clinical endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Differential activity of specific inhibitors of transcription regulating cyclin-dependent kinases in thyroid cancer cells.Endocrine-related cancer · 2025Article
- Targeting CDK2 Confers Vulnerability to Lenvatinib Via Driving Senescence in Anaplastic Thyroid Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Combinatory actions of cytokines induce M2-like macrophages in anaplastic thyroid cancer.American journal of cancer research · 2024Article
- Thyroid Carcinoma with NSD3::NUTM1 Fusion: a Case with Thyrocyte Differentiation and Colloid Production.Endocrine pathology · 2022Article
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- Oncogenic Role of Long Noncoding RNAMALAT1 in Thyroid Cancer Progression through Regulation of the miR-204/IGF2BP2/m6A-MYC Signaling.Molecular therapy. Nucleic acids · 2021Article
- New Horizons: Emerging Therapies and Targets in Thyroid Cancer.The Journal of clinical endocrinology and metabolism · 2021Review
- Targeting transcriptional regulators for treatment of anaplastic thyroid cancer.Journal of cancer metastasis and treatment · 2021Article
- Review
- Chromatin structure regulates cancer-specific alternative splicing events in primary HPV-related oropharyngeal squamous cell carcinoma.Epigenetics · 2020Article
- Novel role of ASH1L histone methyltransferase in anaplastic thyroid carcinoma.The Journal of biological chemistry · 2020Article
- Amino Acid Transporters as Potential Therapeutic Targets in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2020Article
- The combination of BET and PARP inhibitors is synergistic in models of cholangiocarcinoma.Cancer letters · 2020Article
- Hypoxic niches are endowed with a protumorigenic mechanism that supersedes the protective function of PTEN.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- A novel therapeutic approach for anaplastic thyroid cancer through inhibition of LAT1.Scientific reports · 2019Article
- Interference with the bromodomain epigenome readers drives p21 expression and tumor senescence.Cancer letters · 2019Article
- Potentiated anti-tumor effects of BETi by MEKi in anaplastic thyroid cancer.Endocrine-related cancer · 2019Article
- Angiosarcoma and anaplastic carcinoma of the thyroid are two distinct entities: a morphologic, immunohistochemical, and genetic study.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Article
- Unique mutation patterns in anaplastic thyroid cancer identified by comprehensive genomic profiling.Head & neck · 2019Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Context: Recent studies showed that transcription of the MYC gene is driven by the interaction of bromodomain and extraterminal domain (BET) proteins with acetylated histones on chromatin. JQ1, a potent inhibitor that effectively disrupts the interaction of BET proteins with acetylated histones, preferentially suppresses transcription of the MYC gene. We recently reported that JQ1 decreased thyroid tumor growth and improved survival in a mouse model of anaplastic thyroid cancer (ATC) by targeting MYC transcription. The role of MYC in human ATC and whether JQ1 can effectively target MYC as a treatment modality have not been elucidated. Objective: To understand the underlying molecular mechanisms of JQ1, we evaluated its efficacy in human ATC cell lines and xenograft models. Design: We determined the effects of JQ1 on proliferation and invasion in cell lines and xenograft tumors. We identified key regulators critical for JQ1-affected proliferation and invasion of tumor cells. Results: JQ1 markedly inhibited proliferation of four ATC cell lines by suppression of MYC and elevation of p21and p27 to decrease phosphorylated Rb and delay cell cycle progression from the G0/G1 phase to the S phase. JQ1 blocked cell invasion by attenuating epithelial-mesenchymal transition signals. These cell-based studies were further confirmed in xenograft studies in which the size and rate of tumor growth were inhibited by JQ1 via inhibition of p21-cyclin/cyclin-dependent kinase-Rb-E2F signaling. Conclusions: These results suggest targeting of the MYC protein could be a potential treatment modality for human ATC for which effective treatment options are limited.
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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.