Fisetin inhibits migration, invasion and epithelial-mesenchymal transition of LMP1-positive nasopharyngeal carcinoma cells

Li, Rong; Zhao, Yinhai; Chen, Jin; Shao, Songjun; Zhang, Xiujuan

doi:10.3892/mmr.2013.1836

Cited by 26 publications

(19 citation statements)

References 22 publications

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“…The investigation demonstrated that fisetin suppressed the migration and invasion of CNE1-LMP1 cells under non-cytotoxic concentrations. Fisetin up-regulated the epithelial marker, E-cadherin and down-regulated the mesenchymal marker, vimentin accompanied by significant reduction in the levels of the EMT regulator Twist protein [64]. …”

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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“…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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“…Only one published research article has focused on the potential targeting of oncoviruses and EMT in NPC (116). Fisetin is a flavonol, a structurally distinct chemical substance that belongs to the flavonoid group of polyphenols, and it has been reported as having certain anticancer properties.…”

Section: Clinical Application and Anti-emt Targeted Therapymentioning

confidence: 99%

The epithelial–mesenchymal transition (EMT) is regulated by oncoviruses in cancer

et al. 2016

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The epithelial-mesenchymal transition (EMT), defined as transdifferentiation of epithelial cells into mesenchymal cells, is critical for embryonic development, wound healing, tissue regeneration, organ fibrosis, and cancer progression. Recently, the role of EMT in carcinogenesis has attracted much attention. Oncoviruses, including human papillomaviruses (HPVs), Epstein-Barr virus (EBV), and hepatitis B and C viruses (HBVs, HCVs), are known to be involved in the etiology of cancer and have been found to play important roles in cancer metastasis, especially in the EMT process. The HPV encoded oncoproteins E6 and E7 (E6/E7), EBV latent membrane protein-1 and -2A, EBV nuclear antigen, HBV-encoded X antigen, and nonstructural HCV protein 5A are all involved in the regulation of EMT. This review primarily focuses on the role of oncoviruses and their encoded proteins or signaling pathways in the EMT process. Understanding their roles will help us in the development of effective strategies for prevention and treatment of virus-related cancers.-Chen, X., Bode, A. M., Dong, Z., Cao, Y. The epithelialmesenchymal transition (EMT) is regulated by oncoviruses in cancer. FASEB J. 30, 3001-3010 (2016

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Fisetin inhibits migration, invasion and epithelial-mesenchymal transition of LMP1-positive nasopharyngeal carcinoma cells

Cited by 26 publications

References 22 publications

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Exploring the molecular targets of dietary flavonoid fisetin in cancer

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

The epithelial–mesenchymal transition (EMT) is regulated by oncoviruses in cancer

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