ArticleBritish journal of cancer2024
PDZK1 confers sensitivity to sunitinib in clear cell renal cell carcinoma by suppressing the PDGFR-β pathway.
Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Identification of PDGFRB as a prognostic immune-related biomarker in gastric cancer through bioinformatics and clinical analysis.Translational cancer research · 2025Article
- Trends and hotspots in targeted therapy resistance research for renal cell carcinoma: a bibliometric and visualization analysis.Discover oncology · 2025Article
- Review
- Biomarkers in advanced renal cell carcinoma: current practice and future directions.Current opinion in oncology · 2025Review
- PDZK1 inhibits MRP2-mediated oxaliplatin chemosensitivity in hepatocellular carcinoma.Scientific reports · 2025Article
- Microbially produced imidazole propionate impairs prostate cancer progression through PDZK1.Molecular medicine (Cambridge, Mass.) · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundSunitinib has emerged as the primary treatment for advanced or metastatic clear cell renal cell carcinoma (ccRCC) due to its significant improvement in patients' average survival time. However, drug resistance and adverse effects of sunitinib pose challenges to its clinical benefits.
methodsThe differentially expressed genes (DEGs) associated with sunitinib sensitivity and resistance in ccRCC were investigated. Cell counting kit-8, plate colony formation, flow cytometry and subcutaneous xenograft tumor model assays were employed to explore the effects of PDZK1 on ccRCC. Further research on the molecular mechanism was conducted through western blot, co-immunoprecipitation, immunofluorescence co-localization and immunohistochemical staining.
resultsWe elucidated that PDZK1 is significantly downregulated in sunitinib-resistant ccRCC specimens, and PDZK1 negatively regulates the phosphorylation of PDGFR-β and the activation of its downstream pathways through interaction with PDGFR-β. The dysregulated low levels of PDZK1 contribute to inadequate inhibition of cell proliferation, tumor growth, and insensitivity to sunitinib treatment. Notably, our preclinical investigations showed that miR-15b antagomirs enhance sunitinib cytotoxic effects against ccRCC cells by upregulating PDZK1 levels, suggesting their potential in overcoming sunitinib resistance.
conclusionsOur findings establish the miR-15b/PDZK1/PDGFR-β axis as a promising therapeutic target and a novel predictor for ccRCC patients' response to sunitinib treatment.
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