Dietary Lutein Modulates Growth and Survival Genes in Prostate Cancer Cells

Rafi, Mohamed; Kanakasabai, Saravanan; Gokarn, Sarita V; Krueger, Eric G; Bright, John J.

doi:10.1089/jmf.2014.0003

Cited by 58 publications

(41 citation statements)

References 32 publications

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“…However, metastatic breast cancer is heterogeneous and has a high mortality rate due to its inherently aggressive biology. Previous studies have determined that lutein suppresses multiple types of tumor, and the antitumor effects of lutein have been associated with a decline in proliferative signals and growth suppression (21,22,27). Previous studies have focused on the associations between lutein and hypoxia.…”

Section: Discussionmentioning

confidence: 99%

“…Concentrated in the retina, lutein decreases the risk of age-associated macular degeneration due to its anti-oxidative properties (19). Previous studies have demonstrated that lutein exhibits potential antitumor properties in several cancers, including cervical carcinoma, colon cancer and hepatic carcinoma (20)(21)(22). Lutein is involved in cancer initiation and progression by regulating cellular redox status and associated signaling pathways.…”

Section: Lutein Inhibits Proliferation Invasion and Migration Of Hypmentioning

confidence: 99%

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Lutein inhibits proliferation, invasion and migration of hypoxic breast cancer cells via downregulation of HES1

Zhang

Liu

et al. 2018

Int J Oncol

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An intratumoral hypoxic microenvironment is frequently observed in solid tumors, including breast cancer. Lutein, a plant-derived compound and non-vitamin A carotenoid, has been demonstrated to possess multiple protective properties including anti-inflammation, anti-oxidative stress and antitumor effects. The main objective of the present research was to elucidate the involvement of lutein in the production of reactive oxygen species (ROS) under hypoxia, the activation of hairy and enhancer of split 1 (HES1), and the proliferation, invasion and migration of breast cancer cells. The human breast cancer cell lines MDA‑MB‑157 and MCF‑7 were exposed to hypoxic conditions and various concentrations of lutein. An MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay was performed to examine cell proliferation, and Annexin V-fluorescein isothiocyanate/propidium iodide staining was performed to analyze the apoptosis ratio. The levels of hypoxia inducible factor-1α (HIF‑1α), NOTCH signaling molecules, HES1 and epithelial-mesenchymal transition (EMT)-associated factors were examined by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Wound healing and Transwell invasion assays were used to detect the invasion and migration of breast cancer cells. Intracellular ROS levels were examined using 2,7-dichlorodihydrofluorescein-diacetate and flow cytometry. The results revealed that cell proliferation was inhibited by lutein in a dose-dependent manner, and the apoptosis ratio gradually increased with lutein treatment under hypoxia as evident from flow cytometry-based analysis. Exposure to lutein inhibited hypoxia-mediated activation of HIF‑1α, NOTCH signaling and HES1 expression, and suppressed the hypoxia-induced expression of EMT-associated factors. Lutein markedly inhibited the invasion and migration of breast cancer cells under hypoxia. Hypoxia-induced production of ROS was also decreased by lutein. Furthermore, the ROS scavenger N‑acetylcysteine also suppressed hypoxia inducible factor 1α and HES1 expression in breast cancer cells during hypoxia, but hydrogen peroxide (H2O2) levels were increased. Taken together, the results of the present study suggested that lutein may be a novel candidate for the chemoprevention of breast cancer. Furthermore, HES1 may be crucial in mediating the involvement of lutein in the suppression of hypoxia-driven ROS-induced breast cancer progression.

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Section: Discussionmentioning

confidence: 99%

Section: Lutein Inhibits Proliferation Invasion and Migration Of Hypmentioning

confidence: 99%

Lutein inhibits proliferation, invasion and migration of hypoxic breast cancer cells via downregulation of HES1

Zhang

Liu

et al. 2018

Int J Oncol

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“…[82] A study performed on 44 men with no previous incidence of any cardiovascular disease showed an inverse correlation between lutein intake and risk for ischemic stroke when followed up for 8 years. [83] Lutein supplementation was also found to have an inverse [84] Supplementation with 10 or 20 mg/d of lutein has proven to be beneficial for cardiovascular diseases in subjects. [85] Cancer prevention…”

Section: Cardiovascular Healthmentioning

confidence: 99%

Lutein – The Less Explored Carotenoid

Hirdyani¹

2017

WJPR

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Lutein and zeaxanthin are xanthophyll carotenoids found particularly in dark-green leafy vegetables and in egg yolks. They are widely distributed in tissues and are the principal carotenoids in the eye lens and macular region of the retina. Epidemiologic studies depicts an inverse relationship between xanthophyll intake and Retinitis Pigmentosa (RP), cataract and Age-Related Macular Degeneration (ARMD) thus suggesting a protective role of these compounds in the eye. Some observational studies have also shown these xanthophylls may help reduce the risk of certain types of cancer and diabetes. It is also known to have beneficial effects on skin health. Emerging studies suggest as well a potential contribution of lutein and zeaxanthin to the prevention of various cardiovascular diseases too. The use of lutein as a nutritional supplement has been explored in recent years. It is used as a major pharmaceutical but its application as a nutraceutical still needs to be emphasised upon as its industrial application will be very promising in near future. Lutein is a promising biologically active component in the food industry.

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“…Lutein induced a mild decrease in proliferation, improved PPARγ agonistinduced cell-cycle arrest and apoptosis, and altered the expression of growth and apoptosis-associated biomarker genes. 11 Although these studies suggested the involvement of the PPARγ pathway, they did not investigate PPARγ directly or the contribution of the PPARγ pathway to the inhibition of cancer-cell growth by carotenoids. Recently, our experimental results showed that β-carotene enhanced the expression of PPARγ in breast cancer MCF7 cells.…”

Section: Pparγ Activation In Carotenoidinhibited Cancer-cell Prolifermentioning

confidence: 99%

Role of PPARγ in the nutritional and pharmacological actions of carotenoids

Wang¹,

Shi²,

Gu³

et al. 2016

RRBC

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Peroxisome proliferator-activated receptor gamma (PPARγ) has been shown to play an important role in the biological effects of carotenoids. The PPARγ-signaling pathway is involved in the anticancer effects of carotenoids. Activation of PPARγ partly contributes to the growth-inhibitory effects of carotenoids (β-carotene, astaxanthin, bixin, capsanthin, lutein, and lycopene) on breast cancer MCF7 cells, leukemia K562 cells, prostate cancer (LNCaP, DU145, and PC3 cells), and esophageal squamous cancer EC109 cells. PPARγ is the master regulator of adipocyte differentiation and adipogenesis. Downregulated PPARγ and PPARγ-target genes have been associated with the suppressive effects of β-carotene and lycopene on 3T3L1 and C3H10T1/2 adipocyte differentiation and adipogenesis. β-Carotene is cleaved centrally into retinaldehyde by BCO1, the encoding gene being a PPARγ-target gene. Retinaldehyde can be oxidized to retinoic acid and also be reduced to retinol. β-Carotene can also be cleaved asymmetrically into β-apocarotenals and β-apocarotenones by BCO2. The inhibitory effects of β-carotene on the development of adiposity and lipid storage are dependent substantially on BCO1-mediated production of retinoids. The effects of β-carotene on body adiposity were absent in BCO1-knockout mice. Retinoid metabolism is connected with the activity of PPARγ in the control of body-fat reserves. Retinoic acid, retinaldehyde, retinol, and β-apocarotenals exert suppressive effects on preadipocyte differentiation and adipogenesis via downregulation of PPARγ expression in cell culture. The molecular mechanisms underlying retinoic acid effects on adipose-tissue biology and the development of adiposity remain poorly understood. Adiposity can be affected by retinoids through long-lasting effects at critical developmental stages. Retinol saturase increases PPARγ-transcriptional activity and adipocyte differentiation. Other carotenoids that have been reported to suppress adipocyte differentiation and lipid accumulation in the main via modulation of PPARγ and PPARγ-target genes include astaxanthin, bixin, norbixin, β-cryptoxanthin, fucoxanthin and its metabolites, lycopene, apo-10'-lycopenoic acid, siphonaxanthin, and neoxanthin, except paprika pigments. Lutein, lycopene, and paprika carotenoids reduce proinflammatory cytokine levels by an induction of PPARγ in immune tissues and cells. Lycopene, apo-10'-lycopenoic acid, and astaxanthin might prevent atherosclerosis through modifying cholesterol metabolism via increasing PPARγ expression in macrophages.

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Dietary Lutein Modulates Growth and Survival Genes in Prostate Cancer Cells

Cited by 58 publications

References 32 publications

Lutein inhibits proliferation, invasion and migration of hypoxic breast cancer cells via downregulation of HES1

Lutein inhibits proliferation, invasion and migration of hypoxic breast cancer cells via downregulation of HES1

Lutein – The Less Explored Carotenoid

Role of PPARγ in the nutritional and pharmacological actions of carotenoids

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Dietary Lutein Modulates Growth and Survival Genes in Prostate Cancer Cells

Cited by 58 publications

References 32 publications

Lutein inhibits proliferation, invasion and migration of hypoxic breast cancer cells via downregulation of HES1

Lutein inhibits proliferation, invasion and migration of hypoxic breast cancer cells via downregulation of HES1

Lutein – The Less Explored Carotenoid

Role of PPAR&gamma; in the nutritional and pharmacological actions of carotenoids

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Product

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Role of PPARγ in the nutritional and pharmacological actions of carotenoids