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  3. Lipids as Targets for Renal Cell Carcinoma Therapy.
 

Lipids as Targets for Renal Cell Carcinoma Therapy.

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BORIS DOI
10.48350/179252
Publisher DOI
10.3390/ijms24043272
PubMed ID
36834678
Description
Kidney cancer is among the top ten most common cancers to date. Within the kidney, renal cell carcinoma (RCC) is the most common solid lesion occurring. While various risk factors are suspected, including unhealthy lifestyle, age, and ethnicity, genetic mutations seem to be a key risk factor. In particular, mutations in the von Hippel-Lindau gene (Vhl) have attracted a lot of interest since this gene regulates the hypoxia inducible transcription factors HIF-1α and HIF-2α, which in turn drive the transcription of many genes that are important for renal cancer growth and progression, including genes involved in lipid metabolism and signaling. Recent data suggest that HIF-1/2 are themselves regulated by bioactive lipids which make the connection between lipids and renal cancer obvious. This review will summarize the effects and contributions of the different classes of bioactive lipids, including sphingolipids, glycosphingolipids, eicosanoids, free fatty acids, cannabinoids, and cholesterol to renal carcinoma progression. Novel pharmacological strategies interfering with lipid signaling to treat renal cancer will be highlighted.
Date of Publication
2023-02-07
Publication Type
Article
Subject(s)
600 - Technology::610 - Medicine & health
Keyword(s)
cannabinoids cholesterol eicosanoids free fatty acids glycosphingolipids kidney cancer lipids renal cell carcinoma sphingolipids
Language(s)
en
Contributor(s)
Stepanovska Tanturovska, Bisera
Institut für Pharmakologie (PKI)
Institut für Pharmakologie - Gruppe Huwiler
Manaila, Roxana-Cristiana
Institut für Pharmakologie (PKI)
Institut für Pharmakologie - Gruppe Huwiler
Fabbro, Doriano
Huwiler, Andrea
Institut für Pharmakologie (PKI)
Additional Credits
Institut für Pharmakologie (PKI)
Series
International journal of molecular sciences
Publisher
MDPI
ISSN
1422-0067
Access(Rights)
open.access
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