The Inhibitory Effect of Intravesical Fisetin against Bladder Cancer by Induction of p53 and Down‐Regulation of <scp>NF</scp>‐kappa B Pathways in a Rat Bladder Carcinogenesis Model

Li, Jing; Qu, Weixing; Cheng, Yufeng; Sun, Yi; Jiang, Yazhuo; Zou, Tiejun; Wang, Zhiping; Xu, Yan; Zhao, Huacai

doi:10.1111/bcpt.12229

Cited by 43 publications

(31 citation statements)

References 52 publications

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“…Similar effect was observed with fisetin treatment of an autochthonous rat model where bladder cancer was induced by administration of intravesical N-methyl-N-nitrosourea to the animals. Fisetin significantly reduced the incidence of bladder tumors by activating p53 and suppressing NF-κB signaling with modulation of NF-κB target genes involved in cell proliferation and apoptosis [76]. …”

Section: Anti-cancer Activity Of Fisetinmentioning

confidence: 99%

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Syed

Adhami

Khan

et al. 2016

Seminars in Cancer Biology

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The last few decades have seen a resurgence of interest among the scientific community in exploring the efficacy of natural compounds against various human cancers. Compounds of plant origin belonging to different groups such as alkaloids, flavonoids and polyphenols evaluated for their cancer preventive effects have yielded promising data, thereby offering a potential therapeutic alternative against this deadly disease. The flavonol fisetin (3,3′,4′,7-tetrahydroxyflavone), present in fruits and vegetables such as strawberries, apple, cucumber, persimmon, grape and onion, was shown to possess anti-microbial, anti-inflammatory, anti-oxidant and more significantly anti-carcinogenic activity when assessed in diverse cell culture and animal model systems. The purpose of this review is to update and discuss key findings obtained till date from in vitro and in vivo studies on fisetin, with special focus on its anti-cancer role. The molecular mechanism(s) described in the observed growth inhibitory effects of fisetin in different cancer cell types is also summarized. Moreover, an attempt is made to analyze the direction required for future studies that could lead to the development of fisetin as a potent chemopreventive/chemotherapeutic agent against cancer.

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Section: Anti-cancer Activity Of Fisetinmentioning

confidence: 99%

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Syed

Adhami

Khan

et al. 2016

Seminars in Cancer Biology

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“…Effects on other growth regulatory pathways have been noted. After earlier work on cells in culture [Li et al, ], studies in a rat bladder carcinogenesis model indicated that fisetin caused induction of p53 and down‐regulation of NF‐kappa B pathways [Li et al, ].…”

Section: Anticancer Mechanismsmentioning

confidence: 99%

Flavonol Regulation in Tumor Cells

Lea¹

2015

J of Cellular Biochemistry

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Flavonols comprise a group of flavonoid molecules that are widely distributes in fruits and vegetables. There is epidemiological data to suggest that consumption of flavonols can be accompanied by decreased cancer incidence. The anti-oxidant activity of flavonols may have an important role in preventing carcinogenesis. Therapeutic potential of flavonols is indicated by their growth inhibitory action accompanied by a decrease in several hallmarks of cancer such as resistance to apoptosis. Multiple mechanisms of action have been reported for the action of flavonols on cancer cells. Particular emphasis has been directed to inhibitory effects on several protein kinases and on the potential for prooxidant effects. The diversity of actions presents a problem in trying to elucidate primary and secondary effects but it may be a strength of the therapeutic potential of flavonols that it renders development of resistance more difficult for cancer cells. Cancer chemotherapy is usually characterized by the use of drug combinations. Some additive or synergistic combinations have been identified for flavonols and this is an area of ongoing investigation. As with other polyphenolic molecules there have been questions of cellular uptake and bioavailability. Several investigations have been and are being conducted to modify the structures of flavonols with the goal of increasing bioavailability. At present many investigators are sufficiently encouraged by past observations that they are responding to the challenge to optimize the dietary and therapeutic use of flavonols in cancer prevention and treatment.

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“…Previously, fisetin has shown anti-proliferative, anticancer, neuroprotective, and antioxidant activities [10–12]. In recent years, Fisetin has been reported to inhibit cell proliferation, migration and invasion, and induce apoptosis in several cancer types, such as colon cancer [13], glioma cancer [14], lung cancer [15], nasopharyngeal carcinoma [16], prostate cancer [17], and bladder cancer [18] and cervical carcinoma[19]. It also inhibits micro-ophthalmia associated transcription factor (MITF) in melanoma cells and inhibits invasion of melanoma cells via modulation of the MAPK and NF-κB pathways [20–22].…”

Section: Introductionmentioning

confidence: 99%

The Natural Flavonoid Fisetin Inhibits Cellular Proliferation of Hepatic, Colorectal, and Pancreatic Cancer Cells through Modulation of Multiple Signaling Pathways

Youns

Hegazy

2017

PLoS ONE

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Digestive cancers are major causes of mortality and morbidity worldwide. Fisetin, a naturally occurring flavonoid, has been previously shown anti-proliferative, anti-cancer, neuroprotective, and antioxidant activities. In our study, the anti-tumor activities in addition to regulatory effects of fisetin on some cancer cell lines were investigated. Data presented here showed that fisetin induces growth inhibition, and apoptosis in hepatic (HepG-2), colorectal (Caco-2) and pancreatic (Suit-2) cancer cell lines. Gene expression results showed that 1307 genes were significantly regulated in their expression in hepatic and pancreatic cell lines. 350 genes were commonly up-regulated and 353 genes were commonly down-regulated. Additionally, 604 genes were oppositely expressed in both tumor cells. CDK5 signaling, NRF2-mediated oxidative stress response, glucocorticoid signaling, and ERK/MAPK signaling were among most prominent signaling pathways modulating the growth inhibitory effects of fisetin on hepatic and pancreatic cancer cells. The present analysis showed, for the first time, that the anti-tumor effect of fisetin was mediated mainly through modulation of multiple signaling pathways and via activation of CDKN1A, SEMA3E, GADD45B and GADD45A and down-regulation of TOP2A, KIF20A, CCNB2 and CCNB1 genes.

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The Inhibitory Effect of Intravesical Fisetin against Bladder Cancer by Induction of p53 and Down‐Regulation of NF‐kappa B Pathways in a Rat Bladder Carcinogenesis Model

Cited by 43 publications

References 52 publications

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Flavonol Regulation in Tumor Cells

The Natural Flavonoid Fisetin Inhibits Cellular Proliferation of Hepatic, Colorectal, and Pancreatic Cancer Cells through Modulation of Multiple Signaling Pathways

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