Retinoid Receptors

Davidovici, Batya B.; Tüzün, Yalçın; Wolf, Ronni

doi:10.1016/j.det.2007.06.016

Cited by 16 publications

(9 citation statements)

References 39 publications

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“…The classic action of retinoids is thought to involve the activation of nuclear retinoid receptors (26). Our data show, for the first time, that β-carotene significantly promoted and accelerated the development of small airway-derived PAC induced by NNK in vivo by mechanisms that involved non-classical cellular signaling via p-ERK1/2 and p-CREB.…”

Section: Discussionmentioning

confidence: 99%

β-Carotene promotes the development of NNK-induced small airway-derived lung adenocarcinoma

Al-Wadei

Schüller

2009

European Journal of Cancer

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Aim-Beta-carotene has shown cancer preventive effects in preclinical studies while increasing lung cancer mortality in clinical trials. We have shown that β-carotene stimulates cAMP signaling in vitro. Here, we have tested the hypothesis that beta-carotene promotes the development of pulmonary adenocarcinoma (PAC) in vivo via cAMP signaling. Methods: PAC was induced in hamsters with the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) followed by β-carotene for 1.5 years. Incidence, multiplicity and size of lung tumors were recorded and phosphorylated CREB and ERK1/2 in tumour cells determined by Western blots. Cyclic AMP in blood cells was analysed by immunoassays, retinoids in serum and lungs by HPLC. Results: beta-carotene increased lung tumor multiplicity, lung tumour size, blood cell cAMP, serum and lung levels of retinoids and induced p-CREB and p-ERK1/2 in lung tumours. Conclusions:Our data suggest that beta-carotene promotes the development of PAC via increased cAMP signaling.

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Section: Discussionmentioning

confidence: 99%

β-Carotene promotes the development of NNK-induced small airway-derived lung adenocarcinoma

Al-Wadei

Schüller

2009

European Journal of Cancer

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“…Unlike the classic transcriptional effects of retinoids via nuclear retinoid receptors (17,18), the observed signaling responses were rapid, resulting in significant increases of intracellular cAMP and activated PKA within 10-15 min. Moreover, the abrogation of the resulting stimulated cell proliferation via pharmacological downregulation of G· s by CTX in conjunction with a similar effect of the adenylyl cyclase inhibitor SQ clearly point to a direct interaction of retinoid with a G· s -coupled receptor.…”

Section: Discussionmentioning

confidence: 99%

Non-genomic inhibitory signaling of β-carotene in squamous cell carcinoma of the lungs

Al-Wadei

Schüller²

2009

Int J Oncol

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Abstract. Studies have suggested that retinoids prevent lung cancer by interacting with nuclear retinoid receptors. However, clinical trials with ß-carotene increased lung cancer mortality. We recently showed that ß-carotene stimulates the proliferation of small airway-derived adenocarcinoma by increasing cAMP signaling. Here, we have tested the hypothesis that ß-carotene may stimulate squamous cell carcinoma cells via similar mechanisms. We determined the effects of ß-carotene in cell lines from squamous cell carcinomas and large airway epithelia on proliferation by MTT assays in the presence and absence of inhibitors. Signaling via cAMP/PKA was measured by immunoassays and PKA activation assay. Phosphorylated ERK1/2 was determined by Western blotting. ß-carotene significantly inhibited proliferation and phosphorylation of ERK1/2 by G· s -mediated signaling involving adenylyl cyclase, cAMP, PKA and ERK1/2. These findings introduce a non-genomic inhibitory mechanism of ß-carotene and emphasize the need for the development of marker-guided lung cancer prevention.

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“…The expression of retinoid receptors is dependent on anatomic location, presence of inflammation, and disease state 46 . In normal adult skin, 87% of RARs are RAR‐γ, and 13% are RAR‐α (RAR‐β is nearly undetectable) 47 . Regarding RXR's, RXR‐α is 90%, RXR‐γ is very low, and RXR‐β is nearly undetectable 47,48 .…”

Section: Mechanism Of Action Of Retinoidsmentioning

confidence: 99%