ArticleBritish journal of cancer2013
Pazopanib and sunitinib trigger autophagic and non-autophagic death of bladder tumour cells.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Exploring potential VEGF receptor 2 inhibitors: a molecular modeling and pharmacophore-based screening approach.Scientific reports · 2026Article
- Targeting autophagy in dysfunctional tumor vasculature.iScience · 2025Review
- Comparative Neurotoxic Effects of Doxorubicin and Sunitinib: An In Vitro Study on Human Dopaminergic Neuronal Cells.Molecules (Basel, Switzerland) · 2025Article
- Is Autophagy Targeting a Valid Adjuvant Strategy in Conjunction with Tyrosine Kinase Inhibitors?Cancers · 2024Review
- Melatonin alleviates chronic stress-induced hippocampal microglia pyroptosis and subsequent depression-like behaviors by inhibiting Cathepsin B/NLRP3 signaling pathway in rats.Translational psychiatry · 2024Article
- Targeting Pro-Survival Autophagy Enhanced GSK-3β Inhibition-Induced Apoptosis and Retarded Proliferation in Bladder Cancer Cells.Current oncology (Toronto, Ont.) · 2023Article
- Sunitinib versus Pazopanib Dilemma in Renal Cell Carcinoma: New Insights into the In Vitro Metabolic Impact, Efficacy, and Safety.International journal of molecular sciences · 2022Article
- mRNA-miRNA bipartite networks reconstruction in different tissues of bladder cancer based on gene co-expression network analysis.Scientific reports · 2022Article
- Synthesis and Evaluation of Novel 1,2,6-Thiadiazinone Kinase Inhibitors as Potent Inhibitors of Solid Tumors.Molecules (Basel, Switzerland) · 2021Article
- Nephrotoxicity of Anti-Angiogenic Therapies.Diagnostics (Basel, Switzerland) · 2021Review
- Endoplasmic Reticulum Stress and Tumor Microenvironment in Bladder Cancer: The Missing Link.Frontiers in cell and developmental biology · 2021Review
- CRISPR/Cas9 genome-wide loss-of-function screening identifies druggable cellular factors involved in sunitinib resistance in renal cell carcinoma.British journal of cancer · 2020Article
- Vascular mimicry: changing the therapeutic paradigms in cancer.Molecular biology reports · 2020Review
- Drug resistance‑related sunitinib sequestration in autophagolysosomes of endothelial cells.International journal of oncology · 2020Article
- Autophagy modulation in bladder cancer development and treatment (Review).Oncology reports · 2019Review
- Cathepsin B: A sellsword of cancer progression.Cancer letters · 2019Review
- Article
- A novel multikinase inhibitor R8 exhibits potent inhibition on cancer cells through both apoptosis and autophagic cell death.Oncotarget · 2017Article
- Sunitinib induces genomic instability of renal carcinoma cells through affecting the interaction of LC3-II and PARP-1.Cell death & disease · 2017Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTyrosine kinase inhibitors (TKI) such as sunitinib and pazopanib display their efficacy in a variety of solid tumours. However, their use in therapy is limited by the lack of evidence about the ability to induce cell death in cancer cells. Our aim was to evaluate cytotoxic effects induced by sunitinib and pazopanib in 5637 and J82 bladder cancer cell lines.
methodsCell viability was tested by MTT assay. Autophagy was evaluated by western blot using anti-LC3 and anti-p62 antibodies, acridine orange staining and FACS analysis. Oxygen radical generation and necrosis were determined by FACS analysis using DCFDA and PI staining. Cathepsin B activation was evaluated by western blot and fluorogenic Z-Arg-Arg-AMC peptide. Finally, gene expression was performed using RT-PCR Profiler array.
resultsWe found that sunitinib treatment for 24 h triggers incomplete autophagy, impairs cathepsin B activation and stimulates a lysosomal-dependent necrosis. By contrast, treatment for 48 h with pazopanib induces cathepsin B activation and autophagic cell death, markedly reversed by CA074-Me and 3-MA, cathepsin B and autophagic inhibitors, respectively. Finally, pazopanib upregulates the α-glucosidase and downregulates the TP73 mRNA expression.
conclusionOur results showing distinct cell death mechanisms activated by different TKIs, provide the biological basis for novel molecularly targeted approaches.
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