ArticleDiscover oncology2025
Inhibition of colorectal carcinogenesis by sunitinib malate: disruption of the IL-6/STAT3/c-MYC/TWIST/MMP2 autocrine signaling axis.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- A Review on Nanocarrier-Based Strategies for Sunitinib Delivery: Advances in Pharmacokinetic Enhancement and Targeted Theranostics.AAPS PharmSciTech · 2026Review
- Cytokine and chemokine networks in colorectal cancer.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Sunitinib, a multi-targeted receptor tyrosine kinase inhibitor with specificity for VEGFR, KIT, FLT3, and PDGFR, has demonstrated clinical efficacy as a first- to third-line treatment for refractory renal carcinoma. Our previous research indicated that sunitinib malate suppresses intestinal polyp proliferation by downregulating IL-6 mRNA expression, suggesting a potential analogous mechanism in colorectal carcinoma inhibition. This study aimed to elucidate the pharmacological effects and molecular mechanisms of sunitinib malate on colorectal carcinoma using HCT116, RKO, HT29, and SW480 cell lines in vitro and HCT116-derived xenografts in nude mice in vivo. We employed a comprehensive array of experimental techniques, including CCK-8/MTT assays for cell viability, Transwell and/or wound healing assays for migration, and Western blot and immunohistochemistry for protein expression analysis. Our findings demonstrate that sunitinib malate significantly inhibits colorectal cancer cell proliferation and migration in vitro. Moreover, in the xenograft model, sunitinib malate markedly suppressed colorectal tumor growth in vivo. Notably, we observed significant downregulation of c-MYC, TWIST, and MMP2 expression both in vitro and in vivo following sunitinib malate treatment. These results collectively suggest that sunitinib malate exerts its anti-colorectal carcinoma effects, at least in part, by disrupting the autocrine IL-6/STAT3/c-MYC/TWIST/MMP2 signaling axis.
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Registered trials
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