Despite the provision of safe and cost-effective chemopreventive cancer approaches, still there are requirements to enhance their efficiency. The use of dietary agents as phytochemicals plays an imperative role against different human cancer cell lines. Among these novel dietary agents, fisetin (3,3',4',7-tetrahydroxyflavone) is present in different fruits and vegetables such as apple, persimmon, grape, strawberry, cucumber, and onion. Being a potent anticancer agent, fisetin has been used to inhibit stages in the cancer cells (proliferation, invasion), prevent cell cycle progression, inhibit cell growth, induce apoptosis, cause polymerase (PARP) cleavage, and modulate the expressions of Bcl-2 family proteins in different cancer cell lines (HT-29, U266, MDA-MB-231, BT549, and PC-3M-luc-6), respectively. Further, fisetin also suppresses the activation of the PKCα/ROS/ERK1/2 and p38 MAPK signaling pathways, reduces the NF-κB activation, and down-regulates the level of the oncoprotein securin. Fisetin also inhibited cell division and proliferation and invasion as well as lowered the TET1 expression levels. The current review article highlights and discusses the anticancer role of fisetin in cell cultures and animal and human studies. Conclusively, fisetin as a polyphenol with pleiotropic pharmacological properties showed promising anticancer activity in a wide range of cancers. Fisetin suppresses the cancer cell stages, prevents progression in cell cycle and cell growth, and induces apoptosis.
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http://dx.doi.org/10.1002/fsn3.1872 | DOI Listing |
JCI Insight
January 2025
Department of Biomedical Engineering, Oregon Health and Science University, Portland, United States of America.
Spatial profiling of tissues promises to elucidate tumor-microenvironment interactions and generate prognostic and predictive biomarkers. We analyzed single-cell, spatial data from three multiplex imaging technologies: cyclic immunofluorescence (CycIF) data we generated from 102 breast cancer patients with clinical follow-up, and publicly available imaging mass cytometry and multiplex ion-beam imaging datasets. Similar single-cell phenotyping results across imaging platforms enabled combined analysis of epithelial phenotypes to delineate prognostic subtypes among estrogen-receptor positive (ER+) patients.
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January 2025
Herbert Irving Comprehensive Cancer Center, Division of Digestive and Liver, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, United States of America.
Colorectal cancer (CRC) remains a leading cause of cancer death due to metastatic spread. LIN28B is overexpressed in 30% of CRCs and promotes metastasis, yet its mechanisms remain unclear. In this study, we genetically modified CRC cell lines to overexpress LIN28B, resulting in enhanced PI3K/AKT pathway activation and liver metastasis in mice.
View Article and Find Full Text PDFJ Am Chem Soc
January 2025
Department of Chemistry, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, United States.
Lysine demethylases (KDMs) catalyze the oxidative removal of the methyl group from histones using earth-abundant iron and the metabolite 2-oxoglutarate (2OG). KDMs have emerged as master regulators of eukaryotic gene expression and are novel drug targets; small-molecule inhibitors of KDMs are in the clinical pipeline for the treatment of human cancer. Yet, mechanistic insights into the functional heterogeneity of human KDMs are limited, necessitating the development of chemical probes for precision targeting.
View Article and Find Full Text PDFBlood Adv
January 2025
Translational Science and Therapeutics Division, Fred Hutchinson Cancer Center, Seattle, WA.
Cancer Immunol Res
January 2025
University of Chicago, Chicago, IL, United States.
Based on the notion that hypomorphic germline genetic variants are linked to autoimmune diseases, we reasoned that novel targets for cancer immunotherapy might be identified through germline variants associated with greater T-cell infiltration into tumors. Here, we report that while investigating germline polymorphisms associated with a tumor immune gene signature, we identified PKCδ as a candidate. Genetic deletion of PKCδ in mice resulted in improved endogenous antitumor immunity and increased efficacy of anti-PD-L1.
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