ArticleJournal of hematology & oncology2019
Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma.
Article in Journal of hematology & oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 49 citations in OpenAlex.
- Experimental evaluation of Nilotinib and Paclitaxel co-delivered via albumin nanoparticles as a therapeutic strategy for lung squamous cell carcinoma.Clinical and experimental medicine · 2026Article
- Shear Difference: Flow Type Dictates Endothelial Flow-Responsive Gene Programs in a 3-Dimensional-Printed In Vitro Model.Journal of the American Heart Association · 2026Article
- Development of an AQbD-guided sustainable RP-HPLC method for simultaneous quantification of saracatinib and rapamycin in lipid-polymer hybrid nanocarriers.RSC advances · 2026Article
- Artificial Intelligence-Aided Microfluidic Cell Culture Systems.Biosensors · 2025Review
- Dual CDK and MEK Inhibition potentiates CD8Journal of experimental & clinical cancer research : CR · 2025Article
- Superoxide-mediated phosphorylation and stabilization of Mcl-1 by AKT underlie venetoclax resistance in hematologic malignancies.Leukemia · 2025Article
- Fibroblast Activation Protein (FAP)Oncogene · 2025Article
- A Hydrogel-Based Multiplex Coculture Platform for Retinal Component Cells.ACS applied bio materials · 2025Article
- Targeting FDFT1 Reduces Cholesterol and Bile Acid Production and Delays Hepatocellular Carcinoma Progression Through the HNF4A/ALDOB/AKT1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A conserved role for AKT in the replication of emerging flaviviruses in vertebrates and vectors.Virus research · 2024Article
- Capivasertib reverses chemotherapy-induced esophageal cancer resistance via inhibiting Akt-associated Mcl-1 upregulation.Heliyon · 2024Article
- Dual Drug Repurposing: The Example of Saracatinib.International journal of molecular sciences · 2024Review
- Revolutionizing head and neck squamous cell carcinoma treatment with nanomedicine in the era of immunotherapy.Frontiers in immunology · 2024Review
- TMEM25 inhibits monomeric EGFR-mediated STAT3 activation in basal state to suppress triple-negative breast cancer progression.Nature communications · 2023Article
- Targeted therapy for head and neck cancer: signaling pathways and clinical studies.Signal transduction and targeted therapy · 2023Review
- Article
- Mitochondrial regulator ATAD3A: a molecular determinant favoring head and neck cancer development.Oncoscience · 2023Article
- Molecular Basis and Rationale for the Use of Targeted Agents and Immunotherapy in Sinonasal Cancers.Journal of clinical medicine · 2022Review
- Delivery of triptolide: a combination of traditional Chinese medicine and nanomedicine.Journal of nanobiotechnology · 2022Review
- ATAD3A mediates activation of RAS-independent mitochondrial ERK1/2 signaling, favoring head and neck cancer development.Journal of experimental & clinical cancer research : CR · 2022Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSrc, an oncoprotein that drives progression of head and neck squamous cell carcinoma (HNSCC), is commonly hyperactivated in this disease. Unfortunately, the clinical benefit of targeting Src is significantly dampened in HNSCC patients, because the cytotoxic effects of anti-Src therapy and tumor resistance to it are less predictable. Thus, understanding the mechanism of tumor resistance to Src inhibition and seeking a way to overcome it are warranted.
methodsDual drug-loaded nanoparticles (NPs) were developed to co-deliver Src inhibitor saracatinib (AZD0530) and AKT inhibitor capivasertib (AZD5363) into the same population of tumor cells. An orthotopic tongue tumor model was generated to evaluate the in vivo therapeutic effects. Cell growth was determined by CellTiter-Glo® Luminescent Cell Viability Kit, colony formation, and 3D culture, and tumor growth was determined by bioluminescence and tumor size. The molecular changes induced by the treatments were assessed by Western blotting and immunohistochemistry.
resultsCapivasertib inactivated the AKT-S6 signaling and re-sensitized saracatinib-resistant HNSCC cells to saracatinib. Combination of capivasertib with saracatinib suppressed HNSCC growth more efficiently than either drug alone. Cathepsin B-sensitive NPs for co-delivering saracatinib and capivasertib significantly improved the efficacy of tumor repression without increasing side effects, which were due to highly specific tumor-targeting drug delivery system and synergistic anticancer effects by co-inactivation of AKT and Src in HNSCC cells.
conclusionsAddition of AKT blockade improves anti-HNSCC efficacy of anti-Src therapy, and co-delivery of capivasertib and saracatinib by tumor-targeting NPs has the potential to achieve better treatment outcomes than the free drug combination.
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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.