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- W3184800050 endingPage "105784" @default.
- W3184800050 startingPage "105784" @default.
- W3184800050 abstract "It is becoming progressively more understandable that pharmaceutical targeting of drug-resistant cancers is challenging because of intra- and inter-tumor heterogeneity. Interestingly, naturally derived bioactive compounds have unique ability to modulate wide-ranging deregulated oncogenic cell signaling pathways. In this review, we have focused on the available evidence related to regulation of PI3K/AKT/mTOR, Wnt/β-catenin, NF-κB and TRAIL/TRAIL-R by fisetin in different cancers. Fisetin has also been shown to inhibit the metastatic spread of cancer cells in tumor-bearing mice. We have also summarized how fisetin regulated autophagy in different cancers. In addition, this review also covers fisetin-mediated regulation of VEGF/VEGFR, EGFR, necroptosis and Hippo pathway. Fisetin has entered into clinical trials particularly in context of COVID19-associated inflammations. Furthermore, fisetin mediated effects are also being tested in clinical trials with reference to osteoarthritis and senescence. These developments will surely pave the way for full-fledge and well-designed clinical trials of fisetin in different cancers. However, we still have to comprehensively analyze and fully unlock pharmacological potential of fisetin against different oncogenic signaling cascades and non-coding RNAs. Fisetin has remarkable potential as chemopreventive agent and future studies must converge on the identification of additional regulatory roles of fisetin for inhibition and prevention of cancers." @default.
- W3184800050 created "2021-08-02" @default.
- W3184800050 creator A5002433820 @default.
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- W3184800050 creator A5074619520 @default.
- W3184800050 date "2021-10-01" @default.
- W3184800050 modified "2023-10-02" @default.
- W3184800050 title "Cancer chemopreventive role of fisetin: Regulation of cell signaling pathways in different cancers" @default.
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- W3184800050 doi "https://doi.org/10.1016/j.phrs.2021.105784" @default.
- W3184800050 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34302980" @default.