Quercetin inhibits invasion, migration and signalling molecules involved in cell survival and proliferation of prostate cancer cell line (PC‐3)

Kalimuthu, S; Ramachandran, A.; Elumalai, Perumal; Sharmila, Govindaraj; Gunadharini, Dharmalingam Nandhagopal; Banudevi, Sivanantham; Krishnamoorthy, Gunasekar; Benson, Chellakan Selvanesan; Arunakaran, J.

doi:10.1002/cbf.1725

Cited by 101 publications

(54 citation statements)

References 41 publications

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“…In MDA-MB-231 cells, quercetin inhibits invasion and the levels of MMP-3 [161]. In prostate cancer, treatment of PC-3 cells with quercetin decreased the expression of MMP-2/MMP-9 and inhibited invasion and migration, and the mRNA expression of uPA, uPAR, EGF, and EGFR were also downregulated [162,163]. In medulloblastoma, both the Met-induced cell migration and HGF-mediated Akt activation in a medulloblastoma cell line, DAOY, were strongly diminished by quercertin treatment [164].…”

Section: Quercetinmentioning

confidence: 95%

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

Weng

Yen

2012

Cancer Metastasis Rev

187

125

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Cancer metastasis refers to the spread of cancer cells from the primary neoplasm to distant sites, where secondary tumors are formed, and is the major cause of death from cancer. Natural phytochemicals containing phenolic compounds have been widely demonstrated to have the capability to prevent cancer metastasis. Among phenolic compounds, flavonoids are a very large subclass, and they are abundant in food and nutraceuticals. The number of reports demonstrating that flavonoids are an effective natural inhibitor of cancer invasion and metastasis is increasing in the scientific literature. Catechin derivatives, (−)-epigallocatechin-3-gallate, (−)-epigallocatechin, (−)-epicatechin-3-gallate,and (−)-epicatechin, are the most studied compounds in this topic so far; genistein/genistin, silibinin, quercetin, and anthocyanin have also been widely investigated for their inhibitory activities on invasion/metastasis. Other flavonoids in dietary vegetable foods that are responsible for anti-invasive and anti-metastatic activities of tumors include luteolin,apigenin, myricetin, tangeretin, kaempferol, glycitein, licoricidin,daidzein, and naringenin. To effectively overcome the metastatic cascade, including cell-cell attachment, tissue barrier degradation, migration, invasion, cell-matrix adhesion,and angiogenesis, it is essential that a bioactive compound prevent tumor cells from metastasizing. This review summarizes the effects of flavonoids on the metastatic cascade and the related proteins, the in vitro anti-invasive activity of flavonoids against cancer cells, and the effects of flavonoids on antiangiogenic and in vivo anti-metastatic models. The available scientific evidence indicates that flavonoids are a ubiquitous dietary phenolics subclass and exert extensive in vitro anti-invasive and in vivo anti-metastatic activities.

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Section: Quercetinmentioning

confidence: 95%

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

Weng

Yen

2012

Cancer Metastasis Rev

187

125

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“…Many studies have reported inhibition of proliferation and induction of apoptosis in response to various anti-cancer reagents like NO-aspirin [42,43], quercetin [44][45][46], curcumin [47][48][49], and resveratrol [50,51]. Here, we report that compounds 1-3 induced colon cancer cell death via an anti-proliferative/proapoptotic mechanism.…”

Section: Uptake Of Compounds 1-3 Was Detected Via Flow Cytometrymentioning

confidence: 60%

An in vitro study on the effect of synthesized tin(IV) complexes on glioblastoma, colorectal, and skin cancer cell lines

Williams¹,

Lewis-Alleyne²,

Solomon³

et al. 2016

Biomed Res Clin Prac

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Abstract((E)-2-(2-hydroxybenzylideneamino)phenolato-2,2-diphenyl-6-aza-1,3-dioxa-2-stanna- [d,h] dibenzocyclononene, [Sn(Ph 2 SB)] (compound 1, where Ph 2 SB=(E)-2-(2-hydroxybenzylideneamino)phenolato Schiff base) and two novel compounds, [[SnPh 2 (F-azoSB)] (compound 2, where F-azoSB=4-((E)-(4-fluorophenyl) diazenyl)-2-((E)-(2-hydroxyphenylimino)methyl)phenolato Schiff base), [[SnPh 2 (sulf-azoSB)]0.125CHCl 3 (compound 3, where sulfamerazineazosalSB=4-((E)-(4-hydroxy-3-((E)-(2-hydroxyphenylimino)methyl)phenyl)diazenyl)-N-(4-methylpyrimidin-2-yl) benzenesulfonamide Schiff base), and the control compound, cisplatin (compound 4) were analysed to comparatively determine their effect on cancer cell growth. Anti-cancer properties of compounds 1-4 were examined using glioblastoma (U-1242 MG), colorectal (HT-29 and HCT-116), and skin (A431) human cancer cell lines. With regards to human glioblastoma cells, compounds 1 and 3 demonstrated anti-proliferative capacity in the cell line tested. Specifically, compounds 1 and 3 inhibited cell proliferation by 50% at concentrations between 10 and 50 µM. With respect to colon cancer cell lines, the IC 50 values for compounds 1-3 ranged from 3.04 ± 0.98 to 104.51 ± 13.87 µM. In the case of HCT-116, this translates to a 3-to 73-fold inhibitory effect of compounds 1-3 over cisplatin. In all cell lines tested, the chemo-effect was more pronounced with compounds 1-3 than with the control (compound 4); demonstrating that these azo-containing Sn(IV) complexes were more potent than compound 4. The overall effect of compounds 1-3 in the induction of appotosis and the inhibition of proliferation have defined an essential role for these compounds in chemotherapy. IntroductionFrom the late 1960s until the present, there have been significant advances in both the early detection and the treatments of cancer. Despite these advances overall incidences of cancer and deaths from cancer have increased during the same period [1]. These counterintuitive increases have been the impetus for development of new drugs for cancer treatment. In this context the organometallic compounds have been widely investigated as potential anti-tumour agents. Metallocene dihalide complexes Cp 2 MX 2 (where M=titanium, vanadium, niobium, or molybdenum) were the first early transition metal complexes that were shown to have anti-tumour activity. In addition, the organometallic-DNA and organometallic-nucleic acid interactions of these compounds have also been investigated [2][3][4]. More recently, ferricenium salts, organotin, and bismuth complexes have also emerged as examples of organometallic compounds that have been found to exhibit interesting anti-tumour activity [5].The biological activity of organotin compounds has become well known due to their practical applications as fungicides, bactericides, biocides, and pesticides [3,[6][7][8]. It is now well established that organotin compounds are very important in cancer chemotherapy [9] and as potential anti-cancer agents [10][11][12][13]. This is due in part to thei...

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“…and used in Chinese fold medicine) [25], and genistein (an isoflavone found in soy products) [26] inhibit p38 and/or its phosphorylation. Natural compounds that increase p38 and/or p38 phosphorylation in various cancer cell types include the following: glutamine, tyrosine and phenylalanine, and methionine restriction [27], lupulone (a prenylated flavonoid found in hops used in the manufacture of beer) [28], celastrol (a quinone methide triterpene extracted from the root bark of Tripterygium wilfordii, which in Chinese medicine is known as Thunder of God Vine) [29], berberine (an isoquinoline alkaloid with medicinal properties widely distributed in plants, notably Oregon grape, Mahonia aquifolium) [30], quercetin (a flavonol found in fruits, vegetables, leaves and grains) [31], and β-caryophyllene (a bicyclic sessquiterpene found in many essential oils, rosemary, hops, and black pepper) [32]. No consistent pattern is associated with p38 expression and tumor cell migration/invasion and survival.…”

Section: Glucosinolatesmentioning

confidence: 99%

Diet, nutrients, phytochemicals, and cancer metastasis suppressor genes

Meadows

2012

Cancer Metastasis Rev

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The major factor in the morbidity and mortality of cancer patients is metastasis. There exists a relative lack of specific therapeutic approaches to control metastasis, and this is a fruitful area for investigation. A healthy diet and lifestyle not only can inhibit tumorigenesis but also can have a major impact on cancer progression and survival. Many chemicals found in edible plants are known to inhibit metastatic progression of cancer. While the mechanisms underlying antimetastatic activity of some phytochemicals are being delineated, the impact of diet, dietary components, and various phytochemicals on metastasis suppressor genes is underexplored. Epigenetic regulation of metastasis suppressor genes promises to be a potentially important mechanism by which dietary components can impact cancer metastasis since many dietary constituents are known to modulate gene expression. The review addresses this area of research as well as the current state of knowledge regarding the impact of diet, dietary components, and phytochemicals on metastasis suppressor genes.

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Quercetin inhibits invasion, migration and signalling molecules involved in cell survival and proliferation of prostate cancer cell line (PC‐3)

Cited by 101 publications

References 41 publications

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

Flavonoids, a ubiquitous dietary phenolic subclass, exert extensive in vitro anti-invasive and in vivo anti-metastatic activities

An in vitro study on the effect of synthesized tin(IV) complexes on glioblastoma, colorectal, and skin cancer cell lines

Diet, nutrients, phytochemicals, and cancer metastasis suppressor genes

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