Interaction with Type II Estrogen Binding Sites and Antiproliferative Activity of Tamoxifen and Quercetin in Human Non-Small-Cell Lung Cancer

Caltagirone, Sara; Ranelletti, Franco O.; Rinelli, A.; Maggiano, Nicola; Colasante, Antonella; Musiani, Piero; Aiello, Francesca; Piantelli, Mauro

doi:10.1165/ajrcmb.17.1.2728

Cited by 87 publications

(50 citation statements)

References 32 publications

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“…Curcumin is cytostatic in several hormone-dependent (MCF-7 and T-47D) and -independent (SK-BR3, BT-20 and MDA231) breast-tumour cell lines (Mehta et al 1997), while genistein and quercetin, in addition to their antiproliferative action, appear to alter the metastatic potential of rat breast adenocarcinoma cells, measured as a reduced ability to migrate within a collagen matrix (Lu et al 1996). Quercetin inhibits tritiated thymidine uptake and proliferation in several non-small-cell lung carcinoma cell lines and reduces bromodeoxyuridine incorporation in primary lung tumour slices (Caltagirone et al 1997). Quercetin also inhibits ML-3 murine hepatoma cell growth (Chi et al 1997).…”

Section: Cancer Cells In Vitromentioning

confidence: 99%

Plant polyphenols in cancer and heart disease: implications as nutritional antioxidants

Duthie¹,

Duthie²,

Kyle³

2000

Nutr. Res. Rev.

670

400

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Certain dietary antioxidants such as vitamin E and vitamin C are important for maintaining optimum health. There is now much interest in polyphenolic products of the plant phenylpropanoid pathway as they have considerable antioxidant activity in vitro and are ubiquitous in our diet. Rich sources include tea, wine, fruits and vegetables although levels are affected by species, light, degree of ripeness, processing and storage. This confounds the formulation of databases for the estimation of dietary intakes. Most attention to date has focused on the¯avonoids, a generic term which includes chalcones,¯avones,¯avanones,¯avanols and anthocyanins. There is little convincing epidemiological evidence that intakes of polyphenols are inversely related to the incidence of cancer whereas a number of studies suggest that high intakes of¯avonoids may be protective against CHD. In contrast, numerous cell culture and animal models indicate potent anticarcinogenic activity by certain polyphenols mediated through a range of mechanisms including antioxidant activity,

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Section: Cancer Cells In Vitromentioning

confidence: 99%

Plant polyphenols in cancer and heart disease: implications as nutritional antioxidants

Duthie¹,

Duthie²,

Kyle³

2000

Nutr. Res. Rev.

670

400

View full text Add to dashboard Cite

show abstract

“…The anti-inflammatory and antioxidant properties of flavonoids make them likely candidates for evaluation for the treatment of inflammatory diseases including pulmonary diseases [1][2][3][4]. In addition, flavonoids afford cellular protection by inhibiting enzymes involved in cell proliferation and modulating the expression of proteins associated with apoptosis [5].…”

Section: Introductionmentioning

confidence: 99%

Structure-Activity Association of Flavonoids in Lung Diseases

et al. 2014

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Flavonoids are polyphenolic compounds classified into flavonols, flavones, flavanones, isoflavones, catechins, anthocyanidins, and chalcones according to their chemical structures. They are abundantly found in Nature and over 8,000 flavonoids have from different sources, mainly plant materials, have been described. Recently reports have shown the valuable effects of flavonoids as antiviral, anti-allergic, antiplatelet, antitumor, antioxidant, and anti-inflammatory agents and interest in these compounds has been increasing since they can be helpful to human health. Several mechanisms of action are involved in the biological properties of flavonoids such as free radical scavenging, transition metal ion chelation, activation of survival genes and signaling pathways, regulation of mitochondrial function and modulation of inflammatory responses. The anti-inflammatory effects of flavonoids have been described in a number of studies in the literature, but not frequently associated to respiratory disease. Thus, this review aims to discuss the effects of different flavonoids in the control of lung inflammation in some disorders such as asthma, lung emphysema and acute respiratory distress syndrome and the possible mechanisms of action, as well as establish some structure-activity relationships between this biological potential and chemical profile of these compounds.

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“…There are a limited number of studies with conflicting data regarding ERa and ERb expression in human lung cancer and in lung cancer cell lines (Croxtall et al 1994, Caltagirone et al 1997, Omoto et al 2001, Radzikowska et al 2002, Stabile et al 2002, 2005, Hershberger et al 2005 and only two studies directly comparing ER expression in lung cancer specimens and cell lines in males and females (Fasco et al 2002, Mollerup et al 2002. One study reported similar levels of ERa and ERb in females and males (Mollerup et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Gender difference in the activity but not expression of estrogen receptors α and β in human lung adenocarcinoma cells

Dougherty¹,

Mazhawidza²,

Bohn³

et al. 2006

Endocr Relat Cancer

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The higher frequency of lung adenocarcinoma in women smokers than in men smokers suggests a role for gender-dependent factors in the etiology of lung cancer. We evaluated estrogen receptor (ER) a and b expression and activity in human lung adenocarcinoma cell lines and normal lung fibroblasts. Full-length ERa and ERb proteins were expressed in all cell lines with higher ERb than ERa. Although estradiol (E 2 ) binding was similar, E 2 stimulated proliferation only in cells from females, and this response was inhibited by anti-estrogens 4-hydroxytamoxifen (4-OHT) and ICI 182,780. In contrast, E 2 did not stimulate replication of lung adenocarcinoma cells from males and 4-OHT or ICI did not block cell proliferation. Similarly, transcription of an estrogen response element-driven reporter gene was stimulated by E 2 in lung adenocarcinoma cells from females, but not males. Progesterone receptor (PR) expression was increased by E 2 in two out of five adenocarcinoma cell lines from females, but none from males. E 2 decreased E-cadherin protein expression in some of the cell lines from females, as it did in MCF-7 breast cancer cells, but not in the cell lines from males. Thus, ERa and ERb expression does not correlate with the effect of ER ligands on cellular activities in lung adenocarcinoma cells. On the other hand, coactivator DRIP205 expression was higher in lung adenocarcinoma cells from females versus males and higher in adenocarcinoma cells than in normal human bronchial epithelial cells. DRIP205 and other ER coregulators may contribute to differences in estrogen responsiveness between lung adenocarcinoma cells in females and males.

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Interaction with Type II Estrogen Binding Sites and Antiproliferative Activity of Tamoxifen and Quercetin in Human Non-Small-Cell Lung Cancer

Cited by 87 publications

References 32 publications

Plant polyphenols in cancer and heart disease: implications as nutritional antioxidants

Plant polyphenols in cancer and heart disease: implications as nutritional antioxidants

Structure-Activity Association of Flavonoids in Lung Diseases

Gender difference in the activity but not expression of estrogen receptors α and β in human lung adenocarcinoma cells

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