ArticleDrug design, development and therapy2021
Establishment of Sunitinib-Resistant Xenograft Model of Renal Cell Carcinoma and the Identification of Drug-Resistant Hub Genes and Pathways.
Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Recent progress on tyrosine kinase inhibitors resistance in renal cell carcinoma: another brick in the wall?Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Inhibiting stanniocalcin 2 reduces sunitinib resistance of Caki-1 renal cancer cells under hypoxia condition.Annals of medicine and surgery (2012) · 2023Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- Effects of Large Extracellular Vesicles from Kidney Cancer Patients on the Growth and Environment of Renal Cell Carcinoma Xenografts in a Mouse Model.Current issues in molecular biology · 2023Article
- Advances in Renal Cell Carcinoma Drug Resistance Models.Frontiers in oncology · 2022Review
- A novel marker based on necroptosis-related long non-coding RNA for forecasting prognostic in patients with clear cell renal cell carcinoma.Frontiers in genetics · 2022Article
- Research Status of Mouse Models for Non-Small-Cell Lung Cancer (NSCLC) and Antitumor Therapy of Traditional Chinese Medicine (TCM) in Mouse Models.Evidence-based complementary and alternative medicine : eCAM · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSunitinib is the first-line targeted drug for the treatment of advanced renal cell carcinoma (RCC), but its therapeutic potential is limited by premature drug resistance. In an attempt to overcome this limitation, a sunitinib-resistant cell-derived xenograft (CDX) model of clear cell renal cell carcinoma (ccRCC) in vivo was constructed in this study. The molecular mechanism of drug resistance was analyzed using sequencing and bioinformatics tools.
methodsFirst, mice were injected subcutaneously with tumor cells 786-O to create tumors and were simultaneously treated with sunitinib. After three consecutive passages, a drug-resistant xenograft model was obtained. Then, key pathways and genes were identified via second-generation sequencing of the tissue and the examination of differentially expressed genes (DEGs) with bioinformatics tools.
resultsAnalysis of sequencing data revealed that 646 DEGs were upregulated and 465 were downregulated in the drug-resistant tissues when compared with the sensitive tissues. GO showed that the DEGs were significantly enriched in angiogenesis, cell hypoxia response, and apoptosis. KEGG analysis demonstrated that the main pathways were PI3K-Akt, HIF-1, NF-kappa B, and MAPK. Modular analysis of the PPI network indicated that the GO and KEGG analyses of module 1 with the highest ranking were mainly related to ubiquitinase activity. Similarly, the GO and KEGG analyses of the top 10 hub genes were also chiefly linked to ubiquitinase activity. Then, comprehensive expression analysis of the hub genes, and finally, the genes BTRC and TRIM32 were identified, which were consistent in all observations.
conclusionIn this study, through the construction of in vitro models and bioinformatics analysis, the important pathways and key genes related to ccRCC sunitinib resistance were discovered. Among them, ubiquitinase may play an important role in drug resistance and may be a potential therapeutic target and biomarker.
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