Lycopene and the LXRα agonist T0901317 synergistically inhibit the proliferation of androgen-independent prostate cancer cells via the PPARγ-LXRα-ABCA1 pathway

Yang, Chang‐Hsien; Lu, Ya-Ling; Chen, Huei-Yan; Hu, Miao‐Lin

doi:10.1016/j.jnutbio.2011.06.009

Cited by 57 publications

(45 citation statements)

References 46 publications

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“…90,91,93 As mentioned earlier, lycopene increased the expression of PPARγ, LXRα, and ABCA1 and decreased cellular total cholesterol levels in human prostate LNCaP and DU145 cancer cells. 15,16 Lycopene or APO10LA reduced hepatic total cholesterol and elevated cholesterol-efflux genes in BCO2-knockout male mice. 113 It appears that lycopene, apo-10'-lycopenoic acid, and astaxanthin may act as antiatherosclerotic nutrients through modifying cholesterol metabolism.…”

Section: Pparγ In Anti-inflammatory Actions and Modification Of Cholementioning

confidence: 97%

“…15 They observed similar results in androgen-independent prostate cancer DU145 cells, and came to the same conclusion. 16 It has been well known that PPARγ agonists have anticancer activity. 17,18 Taking these aforementioned findings together, it is obvious that upregulation of PPARγ expression is associated with the antiproliferative effects of carotenoids on cancer cells.…”

Section: Pparγ Activation In Carotenoidinhibited Cancer-cell Prolifermentioning

confidence: 99%

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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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Section: Pparγ In Anti-inflammatory Actions and Modification Of Cholementioning

confidence: 97%

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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“…All three can form heterodimers with RXR and LXR (Ferre 2004, Tan et al 2005, Yang et al 2012 and PPARγ can inhibit AR action . PPAR action can also be disrupted by the corepressor NCOR1, similar to AR (Battaglia et al 2010).…”

Section: Peroxisome Proliferator-activated Receptors (Ppars or Nr1c1/mentioning

confidence: 99%

WOMEN IN CANCER THEMATIC REVIEW: New roles for nuclear receptors in prostate cancer

Leach

Powell

Bevan

2016

Endocrine-Related Cancer

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Prostate cancer has, for decades, been treated by inhibiting androgen signalling. This is effective in the majority of patients, but inevitably resistance develops and patients progress to life-threatening metastatic disease -hence the quest for new effective therapies for 'castrate-resistant' prostate cancer (CRPC). Studies into what pathways can drive tumour recurrence under these conditions has identified several other nuclear receptor signalling pathways as potential drivers or modulators of CRPC. The nuclear receptors constitute a large (48 members) superfamily of transcription factors sharing a common modular functional structure. Many of them are activated by the binding of small lipophilic molecules, making them potentially druggable. Even those for which no ligand exists or has yet been identified may be tractable to activity modulation by small molecules. Moreover, genomic studies have shown that in models of CRPC, other nuclear receptors can potentially drive similar transcriptional responses to the androgen receptor, while analysis of expression and sequencing databases shows disproportionately high mutation and copy number variation rates among the superfamily. Hence, the nuclear receptor superfamily is of intense interest in the drive to understand how prostate cancer recurs and how we may best treat such recurrent disease. This review aims to provide a snapshot of the current knowledge of the roles of different nuclear receptors in prostate cancer -a rapidly evolving field of research.

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“…In primary hepatocyte cultures, glucocorticoid increases ABC-A1 expression (40). On the other hand, proliferation is associated with decreased ABC-A1 expression, which may apply to rhuKGF treatment increasing PN-II proliferation (29,38,41). In essence, betamethasone and rhuKGF effects on lung PC homeostasis must be regarded in the context of effects on ABC-A1 as well as ABC-A3 expression, which will have to be addressed in future studies.…”

Section: Pool Sizes Of Newly Synthesized Pc (D 9 -Pc) In Lavaged Lungmentioning

confidence: 99%

Phosphatidylcholine kinetics in neonatal rat lungs and the effects of rhuKGF and betamethasone

Bernhard

Gesche

Raith

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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Lycopene and the LXRα agonist T0901317 synergistically inhibit the proliferation of androgen-independent prostate cancer cells via the PPARγ-LXRα-ABCA1 pathway

Cited by 57 publications

References 46 publications

Role of PPARγ in the nutritional and pharmacological actions of carotenoids

Role of PPARγ in the nutritional and pharmacological actions of carotenoids

WOMEN IN CANCER THEMATIC REVIEW: New roles for nuclear receptors in prostate cancer

Phosphatidylcholine kinetics in neonatal rat lungs and the effects of rhuKGF and betamethasone

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Lycopene and the LXRα agonist T0901317 synergistically inhibit the proliferation of androgen-independent prostate cancer cells via the PPARγ-LXRα-ABCA1 pathway

Cited by 57 publications

References 46 publications

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

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

WOMEN IN CANCER THEMATIC REVIEW: New roles for nuclear receptors in prostate cancer

Phosphatidylcholine kinetics in neonatal rat lungs and the effects of rhuKGF and betamethasone

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Product

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Role of PPARγ in the nutritional and pharmacological actions of carotenoids

Role of PPARγ in the nutritional and pharmacological actions of carotenoids