ArticleCell death and differentiation2021
CRSP8 promotes thyroid cancer progression by antagonizing IKKα-induced cell differentiation.
Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- The roles of IKKα in normal physiology and cancer.Cell communication and signaling : CCS · 2026Review
- IGF2BP2 Drives Thyroid Cancer Dedifferentiation Through m6A-Dependent STAT1 mRNA Destabilization.International journal of biological sciences · 2026Article
- Targeting syndecan-2 inhibits papillary thyroid cancer invasiveness and de-differentiation.BMC endocrine disorders · 2025Article
- SLPI as a dedifferentiation biomarker in BRAFV600E-mutant papillary thyroid cancer.Endocrine connections · 2025Article
- Aurora kinase A promotes epithelial‑mesenchymal transition by regulating P130 and P107 molecules in thyroid cancer cells.Experimental and therapeutic medicine · 2025Article
- CRSP8-driven fatty acid metabolism reprogramming enhances hepatocellular carcinoma progression by inhibiting RAN-mediated PPARα nucleus-cytoplasm shuttling.Journal of experimental & clinical cancer research : CR · 2025Article
- Simultaneous binding of quercetin and catechin to FOXO3 enhances IKKα transcription inhibition and suppression of oxidative stress-induced acute alcoholic liver injury in rats.Journal of advanced research · 2025Article
- Identification of risk factors for high-risk dedifferentiation in papillary thyroid carcinoma and construction of discriminative model.Frontiers in oncology · 2025Article
- Article
- METTL3 regulates thyroid cancer differentiation and chemosensitivity by modulating PAX8.International journal of biological sciences · 2024Article
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- Advances in transcriptomics and proteomics in differentiated thyroid cancer: An updated perspective (Review).Oncology letters · 2023Review
- Transcription factor Zhx2 is a checkpoint that programs macrophage polarization and antitumor response.Cell death and differentiation · 2023Article
- MED27 plays a tumor-promoting role in breast cancer progression by targeting KLF4.Cancer science · 2023Article
- Article
- A novel prognostic model for papillary thyroid cancer based on epithelial-mesenchymal transition-related genes.Cancer medicine · 2022Article
Corrections and comments
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Authors and funding
23 authors at 8 institutions in 1 country.
Funding
Abstract
CRSP8 plays an important role in recruiting mediators to genes through direct interaction with various DNA-bound transactivators. In this study, we uncovered the unique function of CRSP8 in suppressing thyroid cancer differentiation and promoting thyroid cancer progression via targeting IKKα signaling. CRSP8 was highly expressed in human thyroid cancer cells and tissues, especially in anaplastic thyroid cancer (ATC). Knockdown of CRSP8 suppressed cell growth, migration, invasion, stemness, and induced apoptosis and differentiation in ATC cells, while its overexpression displayed opposite effects in differentiated thyroid cancer (DTC) cells. Mechanistically, CRSP8 downregulated IKKα expression by binding to the IKKα promoter region (-257 to -143) to negatively regulate its transcription. Knockdown or overexpression of IKKα significantly reversed the expression changes of the differentiation and EMT-related markers and cell growth changes mediated by CRSP8 knockdown or overexpression in ATC or DTC cells. The in vivo study also validated that CRSP8 knockdown inhibited the growth of thyroid cancer by upregulating IKKα signaling in a mouse model of human ATC. Furthermore, we found that CRSP8 regulated the sensitivity of thyroid cancer cells to chemotherapeutics, including cisplatin and epirubicin. Collectively, our results demonstrated that CRSP8 functioned as a modulator of IKKα signaling and a suppressor of thyroid cancer differentiation, suggesting a potential therapeutic strategy for ATC by targeting CRSP8/IKKα pathway.
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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.