ArticleTranslational cancer research2020
The natural extract degalactotigonin exerts antitumor effects on renal cell carcinoma cells through repressing YAP.
Article in Translational cancer research, 2020. 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, 5 citations in OpenAlex.
- Main chemical constituents and mechanism of anti-tumor action of Solanum nigrum L.Cancer medicine · 2024Review
- Review
- The Hippo pathway: an emerging role in urologic cancers.American journal of clinical and experimental urology · 2021Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe pervasive progression of renal cell carcinoma (RCC) after treatment demands more effective drugs with few side effects. In the present study, we determined whether degalactotigonin (DGT) extracted from
methodsThe effects of DGT on RCC cells were assessed by cell counting kit-8 (CCK-8) assay, flow cytometry, invasion and migration assays and subcutaneous tumor xenograft experiments in nude mice. The related molecular mechanisms were delineated by RNA sequencing (RNA-seq), real-time polymerase chain reaction (PCR), western blotting, coimmunoprecipitation (co-IP) and plasmid transfection.
resultsDGT induced apoptosis and suppressed the proliferation, invasion, migration, and tumorigenicity of RCC cells. Mechanistically, yes-associated protein (YAP) signaling was inactivated, and the expression of YAP and its target genes was reduced in degalactotigonin-treated RCC cells. Additionally, DGT activated phosphorylated large tumor suppressor 1/2 (p-LATS1/2) to phosphorylate YAP, which increased YAP retention in the cytoplasm but decreased the amount of YAP that entered the nuclei of RCC cells. Moreover, DGT impaired the increased aggressive features of RCC cells induced by YAP overexpression.
conclusionsDGT is an effective therapeutic agent, which facilitates the apoptosis and inhibits the proliferation, invasion, migration, and tumorigenicity of RCC cells in a YAP-dependent manner.
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