ArticleJournal of bioenergetics and biomembranes2023
USP10 suppresses ABCG2-induced malignant characteristics of doxorubicin-resistant thyroid cancer by inhibiting PI3K/AKT pathway.
Article in Journal of bioenergetics and biomembranes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- Review
- Macrophage-Derived Transcriptional Signatures Predict Prognosis and Drug Sensitivity in Thyroid Cancer: Integrative Analysis and Experimental Validation of SMYD3.ImmunoTargets and therapy · 2026Article
- Ubiquitin-Specific Protease 10: A New Target in Tumor Immune Escape.Cancer control : journal of the Moffitt Cancer CenterReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin (DOX) is the most extensively used drug in the chemotherapy of thyroid cancer (TC). However, the existence of DOX resistance is not conducive to TC treatment. Here, we investigated the role of USP10 in DOX-resistant TC and explored the underlying molecular mechanism. CCK-8 assay was used to measure cell viability in thyroid cancer FTC133 and DOX-resistant FTC133-DOX cells. RT-qPCR and western blot were used to evaluate USP10 expression. Cell migration, invasion, and apoptotic assays were conducted. Western blot was used to detect cellular signaling proteins, EMT-related proteins, and apoptosis-related proteins. We found a lower expression of USP10 in the human TC cell line FTC133 as compared to the normal human thyroid Htori-3 cells. Notably, USP10 expression was further reduced in DOX-resistant (FTC133-DOX) cells compared to the FTC133 cells. FTC133-DOX cells had increased invasion, migration, and EMT properties while less apoptosis by activating the PI3K/AKT pathway. Interestingly, overexpressing USP10 increased the chemosensitivity of FTC133 cells to DOX therapy. Overexpressing USP10 inhibited invasion, migration, and EMT properties of FTC133-DOX cells and promoted apoptosis. Mechanistically, overexpressing USP10 inhibited PI3K/AKT pathway by activating PTEN. Furthermore, overexpressed USP10 controlled all these processes by downregulating ABCG2. This study demonstrates that USP10 could reduce DOX-induced resistance of TC cells to DOX therapy and could suppress TC malignant behavior by inhibiting the PI3K/AKT pathway. Furthermore, USP10 targeted ABCG2 to inhibit all these malignant processes, therefore, either increasing USP10 expression or inhibiting ABCG2 could be used as novel targets for treating DOX-resistant thyroid cancer.
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Registered trials
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