ArticleCell cycle (Georgetown, Tex.)
Drug-induced inhibition of HMGA and EZH2 activity as a possible therapy for anaplastic thyroid carcinoma.
Article in Cell cycle (Georgetown, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Complicated crosstalk between HMGA and non-coding RNAs modulates hallmarks of cancer.Cancer cell international · 2025Review
- HMGA1 regulates trabectedin sensitivity in advanced soft-tissue sarcoma (STS): A Spanish Group for Research on Sarcomas (GEIS) study.Cellular and molecular life sciences : CMLS · 2024Article
- Modulating gene expression as a strategy to investigate thyroid cancer biology.Archives of endocrinology and metabolism · 2024Review
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
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Abstract
Anaplastic thyroid carcinoma (ATC) is one of the most aggressive and lethal neoplasms in humans, and just limited progresses have been made to extend patient survival and decrease ATC-associated mortality. Thus, the identification of novel therapeutic strategies for treating ATC is needed. Recently, our group has identified two proteins with oncogenic activity, namely HMGA1 and EZH2, with pivotal roles in ATC cancer progression. Therefore, we tested the ability of trabectedin, a HMGA1-targeting drug, and GSK126, an inhibitor of EZH2 enzymatic activity, to impair cell viability of four ATC-derived cell lines. In the present study, we first confirmed the overexpression of
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