ArticleInternational journal of biological sciences2025
Microtubule dynamics is a therapeutic vulnerability in VHL-deficient renal cell carcinoma.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- DNA methyltransferase inhibition is a therapeutic vulnerability in VHL-deficient renal cell carcinoma cells.Experimental & molecular medicine · 2026Article
- Microtubule regulation in cancer cells.Frontiers in cell and developmental biology · 2025Article
- Modulation of the cytoskeleton for cancer therapy.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
Von Hippel-Lindau (VHL) is a tumor suppressor frequently mutated in renal cell carcinoma (RCC) and its loss has been considered as a target for therapeutic exploitation. In an effort to identify therapeutic vulnerabilities in VHL-deficient RCC, we found that SKPin C1, a SKP2 inhibitor, exhibited synthetic lethal effects on VHL-deficient RCC cells. SKPin C1 selectively disrupted spindle assembly in VHL-deficient RCC, leading to the induction of mitotic arrest and death. These effects were independent of its inhibitory action on SKP2. Our in-depth biochemical and molecular interaction studies reveal that SKPin C1 binds to tubulin and inhibits microtubule polymerization. Interestingly, anti-microtubule effect of SKPin C1 was much more pronounced in VHL-deficient RCC cells. Further mechanistic studies on the synthetic lethality reveal that VHL loss alters microtubule dynamics in cells, promoting microtubule growth speed while reducing stability. Treatment of VHL-deficient RCC cells with SKPin C1 or other microtubule destabilizers strongly suppressed microtubule growth and reduced the levels of GTP-tubulin and acetylated microtubules, resulting in selective vulnerability in VHL-deficient RCC. Taken together, our study suggests that microtubule dynamics is a therapeutic vulnerability in VHL-deficient RCC and provides a rationale for the combination treatment of VHL-deficient RCC with anti-microtubule agents and RCC targeted therapies.
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