ArticleInternational journal of oncology2019
Sorafenib inhibits vascular endothelial cell proliferation stimulated by anaplastic thyroid cancer cells regardless of BRAF mutation status.
Article in International journal of oncology, 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, 31 citations in OpenAlex.
- Convergent Mechanistic Pathways Driving the Anaplastic Phenotype in Thyroid Cancer.International journal of molecular sciences · 2026Review
- Ultrasound stimulated microbubble cavitation promoted the anticancer effect of Lenvatinib on anaplastic thyroid cancer.BMC pharmacology & toxicology · 2025Article
- MOF enhances the sensitivity and selectivity of sorafenib as an anticancer drug against hepatocellular carcinoma and colorectal cancer in vitro.Scientific reports · 2025Article
- LINC00162 silencing enhances sorafenib sensitivity and inhibits thyroid cancer cells progression through modulation of MAPK signaling and apoptosis.Scientific reports · 2025Article
- Inflammation-associated drug resistance and tumor growth in TNBC.Frontiers in immunology · 2025Review
- Unlocking the promise of MANF in diseases: Mechanistic insights and therapeutic potentials.Molecular biology reports · 2024Review
- Recent updates on potential of VEGFR-2 small-molecule inhibitors as anticancer agents.RSC advances · 2024Review
- Recent Trends and Potential of Radiotherapy in the Treatment of Anaplastic Thyroid Cancer.Biomedicines · 2024Review
- RETRACTED: Potential Antitumor Activity of Combined Lycopene and Sorafenib against Solid Ehrlich Carcinoma via Targeting Autophagy and Apoptosis and Suppressing Proliferation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Nomogram predicts risk and prognostic factors for lung metastasis of anaplastic thyroid carcinoma: a retrospective study in the Surveillance Epidemiology and End Results (SEER) database.Translational cancer research · 2023Article
- Stromal cells in the tumor microenvironment: accomplices of tumor progression?Cell death & disease · 2023Review
- Review
- Identification of pan-kinase-family inhibitors using graph convolutional networks to reveal family-sensitive pre-moieties.BMC bioinformatics · 2022Article
- Advances in targeted therapy for anaplastic thyroid carcinoma.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Review
- Longitudinal assessment of B-RAF V595E levels in the peripheral cell-free tumor DNA of a 10-year-old spayed female Korean Jindo dog with unresectable metastatic urethral transitional cell carcinoma for monitoring the treatment response to a RAF inhibitor (sorafenib).The veterinary quarterly · 2021Article
- Crosstalk between H1975 tumor cells and platelets to induce the proliferation, migration and tube formation of vascular endothelial cells.Oncology letters · 2021Article
- Anaplastic Thyroid Carcinoma: Current Issues in Genomics and Therapeutics.Current oncology reports · 2021Review
- Cetuximab-conjugated perfluorohexane/gold nanoparticles for low intensity focused ultrasound diagnosis ablation of thyroid cancer treatment.Science and technology of advanced materials · 2021Article
- Zebrafish Models of Cancer Therapy-Induced Cardiovascular Toxicity.Journal of cardiovascular development and disease · 2021Review
- Precise engineering of Gemcitabine prodrug cocktails into single polymeric nanoparticles delivery for metastatic thyroid cancer cells.Drug delivery · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic thyroid cancer (ATC) is a rare refractory disease, frequently associated with BRAF mutations and aberrant vascular endothelial growth factor (VEGF) secretion. The antitumor effects of sorafenib were evaluated, and its mechanisms of action were investigated. Four human ATC cell lines were used: OCUT‑4, which possesses a BRAF mutation; OCUT‑6 and ACT‑1, which carry NRAS mutations; and OCUT‑2, which possesses mutations in BRAF and PI3KCA. The viability of Sorafenib was evaluated by MTT assay. In order to examine the inhibitory effect of Sorafenib on intracellular signal transduction, expression of mitogen‑activated protein kinase kinase was examined by western blotting. In addition, cell cycle analysis was performed using flow cytometry. The inhibitory effects of sorafenib on the growth of ATC cells and human umbilical vein endothelial cells (HUVECs) stimulated with conditioned media from ATC cells were examined. Sorafenib inhibited the viability of OCUT‑4 more effectively than other ATC cell lines; these effects may have been mediated cytostatically by suppressing mitogen‑activated protein kinase kinase phosphorylation. Conversely, similar suppression was not observed in OCUT‑6 cells, which possess an NRAS mutation. The four cell lines secreted different quantities of VEGF, and the proliferation of HUVECs was differentially stimulated by their conditioned media. Both anti‑VEGF antibody and sorafenib prevented this stimulation of proliferation. In conclusion, sorafenib more effectively inhibited RAF‑generated growth signals in ATC cells compared with signals generated by its upstream gene, RAS. ATC cells stimulated the growth of HUVECs via humoral factors, including VEGF; this effect was clearly inhibited by sorafenib. The present findings highlighted the potential of sorafenib for the treatment of ATC and provided insight into its mechanism of action.
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