Regulation of Retinoic Acid Receptor Expression in Dermal Fibroblasts

Tsou, Hui C.; Lee, Xinhua; Pan, Seong; Peacocke, Monica

doi:10.1006/excr.1994.1061

Cited by 23 publications

(13 citation statements)

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“…Our RT-PCR indicated significant down-regulation of RAR␣, which is likely involved in the stimulation of NIS. 5 The inhibition of RAR␣ mRNA by tRA is consistent with reports in different cell lines and tissues (41)(42)(43). In addition, tRA induces degradation of RAR ␣ and ␥ in MCF-7 cells in vitro by ubiquitination (44).…”

Section: Discussionsupporting

confidence: 87%

Systemic Retinoic Acid Treatment Induces Sodium/Iodide Symporter Expression and Radioiodide Uptake in Mouse Breast Cancer Models

Kogai¹,

Kanamoto²,

Lisa³

et al. 2004

Cancer Research

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Lactating breast tissue and some breast cancers express the sodium/ iodide symporter (NIS) and concentrate iodide. We recently demonstrated that all-trans retinoic acid (tRA) induces both NIS gene expression and iodide accumulation in vitro in well-differentiated human breast cancer cells (MCF-7). In the present study, we investigated the in vivo efficacy and specificity of tRA-stimulated iodide accumulation in mouse breast cancer models. Immunodeficient mice with MCF-7 xenograft tumors were treated with systemic tRA for 5 days. Iodide accumulation in the xenograft tumors was markedly increased, ϳ15-fold greater than levels without treatment, and the effects were tRA dose dependent. Iodide accumulation in other organs was not significantly influenced by tRA treatment. Significant induction of NIS mRNA and protein in the xenograft tumors was observed after tRA treatment. Iodide accumulation and NIS mRNA expression were also selectively induced in breast cancer tissues in transgenic mice expressing the oncogene, polyoma virus middle T antigen. These data demonstrate selective induction of functional NIS in breast cancer by tRA. Treatment with short-term systemic retinoic acid, followed by radioiodide administration, is a potential tool in the diagnosis and treatment of some differentiated breast cancer.

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Section: Discussionsupporting

confidence: 87%

Systemic Retinoic Acid Treatment Induces Sodium/Iodide Symporter Expression and Radioiodide Uptake in Mouse Breast Cancer Models

Kogai¹,

Kanamoto²,

Lisa³

et al. 2004

Cancer Research

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“…The PREP9 construct was driven by an RSV promoter and used an SV40-derived poly A tail. For the RAR␤2 reporter construct, pXP-D2 containing 1.6 kb of the 5Ј regulatory sequence of the RAR␤2 promoter [Ϫ1.6 kb to ϩ156 (PstI-BamHI) including the RARE and the TATA box] was inserted into the XhoI-Bg/II site of the promoterless luciferase reporter plasmid, pXP2 (33,34).…”

Section: Methodsmentioning

confidence: 99%

β-Carotene and β-Apo-14′-Carotenoic Acid Prevent the Reduction of Retinoic Acid Receptor β in Benzo[a]pyrene-Treated Normal Human Bronchial Epithelial Cells

Prakash

Liu

et al. 2004

The Journal of Nutrition

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Low-dose ␤-carotene (BC) supplementation, such as would be provided by daily consumption of ϳ5-9 servings of fruits and vegetables, has no apparent detrimental effects, but rather appears to have a protective effect against cigarette smoke-induced lung lesions in ferrets. In the present study, we investigated the effects of BC, ␤-apo-14Ј-carotenoic acid (14ЈCA), or benzo[a]pyrene (BP; a primary lung carcinogen from cigarette smoke) treatments, either alone or in combination, on cell growth and expression of the retinoic acid receptor (RAR) of normal human bronchial epithelial (NHBE) cells. We found that both BC and 14ЈCA inhibited the growth of NHBE cells (P Ͻ 0.05) with or without BP. The level of RAR␤, a tumor suppressor, but not R〈R␣ or R〈R␥, was reduced by 50% in the NHBE cells treated with BP. However, treatment with either BC or 14ЈCA significantly induced the expression of RAR␤ in the NHBE cells, and prevented the reduction of RAR␤ by BP. Furthermore, 14ЈCA transactivated the RAR␤ promoter primarily via its conversion to retinoic acid (RA). In the presence of 3-mercaptopropionic acid, an inhibitor of fatty acid oxidation, both RA formation and transactivation activity from 14ЈCA were decreased. These observations indicate that the growth inhibitory effects of BC and ␤-apo-carotenoic acid are through their conversion to RA and upregulation of RAR␤. J. Nutr. 134: 667-673, 2004.

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“…Total RNA from each lymphoblastoid cell line was isolated with 4 M guanidine isothiocyanate and purified through a cushion of 5.7 M cesium chloride as described (Tsou et al 1994). RT-PCRs were performed using the Titan One Tube RT-PCR system (Boehringer Mannheim).…”

Section: Rna Isolation and Reverse Transcription-polymerase Chain Reamentioning

confidence: 99%

The genetic basis of Cowden's syndrome: three novel mutations in PTEN/MMAC1/TEP1

Tsou¹,

Ping²,

Xie³

et al. 1998

Human Genetics

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Cowden's syndrome (CS) is an autosomal dominant disorder associated with an increased risk of developing benign and malignant tumors in a variety of tissues, including the skin, thyroid, breast and brain. Women with CS are felt to have an increased risk of developing breast cancer, and virtually all women with CS develop bilateral fibrocystic disease of the breast. Recently, a series of germline mutations have been identified from CS families in a gene known as PTEN/MMAC1/TEP1. In this study, we used heteroduplex analysis and direct sequencing analysis and identified three novel germline mutations in the PTEN/MMAC1/TEP1 coding sequence from unrelated individuals with CS. We report a de novo transition (T-->C) at nucleotide 335 in exon 5. This missense mutation resulted in a leucine to proline (CTA to CCA) change at codon 112. We also describe a novel splice site mutation (801+2T-->G) in intron 7 that caused exon skipping in PTEN/MMAC1/TEP1 mRNA. The third mutation we report is a missense mutation, consisting of a transition (T-->C) at nucleotide 202 in exon 3, resulting in a tyrosine to histidine (TAC to CAC) change at codon 68. Finally, we also detected a rare polymorphism in exon 7 of the PTEN/MMAC1/TEP1 coding sequence. These data confirm the observation that mutations of the PTEN/MMAC1/TEP1 coding sequence are responsible for at least some cases of CS, and further define the spectrum of mutations in this autosomal dominant disorder.

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Regulation of Retinoic Acid Receptor Expression in Dermal Fibroblasts

Cited by 23 publications

References 0 publications

Systemic Retinoic Acid Treatment Induces Sodium/Iodide Symporter Expression and Radioiodide Uptake in Mouse Breast Cancer Models

Systemic Retinoic Acid Treatment Induces Sodium/Iodide Symporter Expression and Radioiodide Uptake in Mouse Breast Cancer Models

β-Carotene and β-Apo-14′-Carotenoic Acid Prevent the Reduction of Retinoic Acid Receptor β in Benzo[a]pyrene-Treated Normal Human Bronchial Epithelial Cells

The genetic basis of Cowden's syndrome: three novel mutations in PTEN/MMAC1/TEP1

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