ArticleInternational journal of molecular sciences2021
Molecular and Functional Analysis of Sunitinib-Resistance Induction in Human Renal Cell Carcinoma Cells.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- CircLAMA5 traps Sam68 in the cytoplasm to regulate alternative splicing and drive sunitinib resistance in ccRCC.Oncogene · 2026Article
- Transcriptional Regulation of Receptor-Mediated Mitophagy in Sunitinib-Resistant Renal Cancer Cells: Response to Succinic Acid.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Review
- The novel hydrogen-PT2385-silncARSR nanocomplex impairs tumor angiogenesis and mitochondrial activity in sunitinib-resistant renal cancer.Materials today. Bio · 2025Article
- Loss of SETD2 in wild-type VHL clear cell renal cell carcinoma sensitizes cells to STF-62247 and leads to DNA damage, cell cycle arrest, and cell death characteristic of pyroptosis.Molecular oncology · 2025Article
- Microflow Liquid Chromatography Coupled to Multinozzle Electrospray Ionization for Improved Lipidomics Coverage of 3D Clear Cell Renal Cell Carcinoma.Analytical chemistry · 2025Article
- Metabolomics Reveals Tyrosine Kinase Inhibitor Resistance-Associated Metabolic Events in Human Metastatic Renal Cancer Cells.International journal of molecular sciences · 2024Article
- Molecular and functional characterization of reversible-sunitinib-tolerance state in human renal cell carcinoma.Journal of cellular and molecular medicine · 2024Article
- Inhibiting stanniocalcin 2 reduces sunitinib resistance of Caki-1 renal cancer cells under hypoxia condition.Annals of medicine and surgery (2012) · 2023Article
- Modulation of lncRNA links endothelial glycocalyx to vascular dysfunction of tyrosine kinase inhibitor.Cardiovascular research · 2023Article
- Multifunctional Nanoplatform Based on Sunitinib for Synergistic Phototherapy and Molecular Targeted Therapy of Hepatocellular Carcinoma.Micromachines · 2023Article
- Mechanisms of tyrosine kinase inhibitor resistance in renal cell carcinoma.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Concomitant Use of Sulforaphane Enhances Antitumor Efficacy of Sunitinib in Renal Cell Carcinoma In Vitro.Cancers · 2022Article
- 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
- Advances in Renal Cell Carcinoma Drug Resistance Models.Frontiers in oncology · 2022Review
- Article
- Drug Repurposing to Identify a Synergistic High-Order Drug Combination to Treat Sunitinib-Resistant Renal Cell Carcinoma.Cancers · 2021Article
- Establishment of Sunitinib-Resistant Xenograft Model of Renal Cell Carcinoma and the Identification of Drug-Resistant Hub Genes and Pathways.Drug design, development and therapy · 2021Article
- Exploring oncology treatment strategies with tyrosine kinase inhibitors through advanced 3D models (Review).Medicine internationalReview
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance in clear cell renal cell carcinoma (ccRCC) against sunitinib is a multifaceted process encompassing numerous molecular aberrations. This induces clinical complications, reducing the treatment success. Understanding these aberrations helps us to select an adapted treatment strategy that surpasses resistance mechanisms, reverting the treatment insensitivity. In this regard, we investigated the dominant mechanisms of resistance to sunitinib and validated an optimized multidrug combination to overcome this resistance. Human ccRCC cells were exposed to single or chronic treatment with sunitinib to obtain three resistant clones. Upon manifestation of sunitinib resistance, morphometric changes in the cells were observed. At the molecular level, the production of cell membrane and extracellular matrix components, chemotaxis, and cell cycle progression were dysregulated. Molecules enforcing the cell cycle progression, i.e., cyclin A, B1, and E, were upregulated. Mass spectrometry analysis revealed the intra- and extracellular presence of
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