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A comprehensive view on the fisetin impact on colorectal cancer in animal models: Focusing on cellular and molecular mechanisms

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Animal Models and Experimental Medicine 2024年第05期 591-605页

作者： Mohammad Yasin Zamanian Niloofar Taheri Montather F.Ramadan Yasser Fakri Mustafa Safa Alkhayyat Klunko Nataliya Sergeevna Hashem O.Alsaab ahmed hjazi Farnoosh Molavi Vasei Siamak Daneshvar Department of Physiology School of Medicine Hamadan University of Medical Sciences Department of Pharmacology and Toxicology School of Pharmacy Hamadan University of Medical Sciences School of Medicine Shahroud University of Medical Sciences College of Dentistry Al-Ayen University Department of Pharmaceutical Chemistry College of Pharmacy University of Mosul College of Pharmacy The Islamic University Department of Training of Scientific and Scientific-Pedagogical Personnel Russian New University Department of Pharmaceutics and Pharmaceutical Technology Taif University Department of Medical Laboratory College of Applied Medical Sciences Prince Sattam bin Abdulaziz University Department of Clinical Biochemistry School of Medicine Rafsanjan University of Medical Sciences Department of Surgery School of Medicine Hamadan University of Medical Sciences

Flavonoids, including fisetin, have been linked to a reduced risk of colorectal cancer(CRC) and have potential therapeutic applications for the condition. Fisetin, a natural flavonoid found in various fruits and vegetables, has shown promise in managing CRC due to its diverse biological activities. It has been found to influence key cell signaling pathways related to inflammation, angiogenesis, apoptosis, and transcription *** results of this study demonstrate that fisetin induces colon cancer cell apoptosis through multiple mechanisms. It impacts the p53 pathway, leading to increased levels of p53 and decreased levels of murine double minute 2, contributing to apoptosis induction. Fisetin also triggers the release of important components in the apoptotic process, such as second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI and cytochrome c. Furthermore, fisetin inhibits the cyclooxygenase-2 and wingless-related integration site(Wnt)/epidermal growth factor receptor/nuclear factor kappa B signaling pathways, reducing Wnt target gene expression and hindering colony formation. It achieves this by regulating the activities of cyclin-dependent kinase 2 and cyclin-dependent kinase 4, reducing retinoblastoma protein phosphorylation, decreasing cyclin E levels, and increasing p21 levels, ultimately influencing E2 promoter binding factor 1 and cell division cycle 2(CDC2) protein levels. Additionally, fisetin exhibits various effects on CRC cells, including inhibiting the phosphorylation of Y-box binding protein 1 and ribosomal S6 kinase, promoting the phosphorylation of extracellular signal-regulated kinase 1/2, and disrupting the repair process of DNA double-strand breaks. Moreover, fisetin serves as an adjunct therapy for the prevention and treatment of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α(PIK3CA)-mutant CRC, resulting in a reduction in phosphatidylinositol-3 kinase(PI3K) expressio

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