Cell Type-specific Expression of β-Carotene 15,15′-Mono-oxygenase in Human Tissues

Lindqvist, Anna-Karin; Andersson, Stefan

doi:10.1177/002215540405200407

Cited by 73 publications

(64 citation statements)

References 36 publications

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“…In 2004 Lindquist and Andersson revealed that the normal endometrium expresses BCO1, the enzyme that catalyses the first step in the conversion of dietary provitamin A carotenoids to vitamin A. Thus it may be responsible for local synthesis of retinol from the carotenoids accumulated in the uterus in cases when their dietary supply is insufficient [26].…”

Section: Discussionmentioning

confidence: 99%

Dietary carotenoids in normal and pathological tissues of corpus uteri.

Czeczuga-Semeniuk

Wołczyński²

2008

Folia Histochem Cytobiol.

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Carotenoids and retinyl esters are the source of vitamin A in the human body and its natural derivatives takes part in the regulation of cell replication and differentiation in the human endometrium, may induce the leiomyoma growth and has a role in differentiation of endometrial adenocarcinoma. The aim of the study was to demonstrate the presence of carotenoids in tissues from the normal uterus and from various tumors of the uterine corpus, as well as to compare the total content, major carotenoids and % of carotenoids belonging to the provitamin A group between the tissues examined. Using three independent methods of chromatography (CC, TLC, HPLC) we analysed 140 human samples. We identified 13 carotenoids belonging to the eg. provitamin A group and epoxy carotenoids. In all the samples β-carotene, β-cryptoxanthin, lutein, neoxanthin, violaxanthin and mutatoxanthin were isolated. In normal tissues, the mean carotenoid content was the highest in the follicular phase endometrium (9.9 μg/g), while the highest percentage of carotenoids belonging to provitamin A group was found in the luteal phase (18.2%). In the pathological group, the highest mean values were demonstrated for epithelial lesions (8.0 μg/g), and within this group -in endometrioid adenocarcinoma (10.8 μg/g). In both groups, violaxanthin, β-cryptoxanthin, lutein epoxide and mutatoxanthin were the predominant carotenoids. We have demonstrated that all uterine tissues show a concentration of β-carotene and β-cryptoxanthin, being the source of vitamin A. The highest total values of carotenoids obtained in the group of endometrioid adenocarcinoma seem to confirm certain enzymatic defects in carotenoid metabolism in the course of the neoplastic process or some metabolic modifications. The finding of astaxanthin -the major antioxidant among carotenoids -in 63% of tissues examined is also significant.

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Section: Discussionmentioning

confidence: 99%

Dietary carotenoids in normal and pathological tissues of corpus uteri.

Czeczuga-Semeniuk

Wołczyński²

2008

Folia Histochem Cytobiol.

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“…Expression of the bco1 and bco2 genes overlaps in the human gastrointestinal tract, but bco2, additionally, is expressed in several tissues neither known to be sensitive to vitamin A deficiency nor to express bco1 (20,21). The discovery that BCO1-null mice cannot metabolize b-carotene to vitamin A despite intact bco2 expression (22) implicated BCO2 in biological processes other than vitamin A synthesis.…”

Section: Introductionmentioning

confidence: 99%

“…BCO2 is expressed in normal prostate epithelium (20,21). The observation that lycopene levels are significantly higher in cancerous than in normal or benign prostate (23) prompted our speculation that BCO2-mediated lycopene metabolism may be impaired in prostate cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial β-Carotene 9′,10′ Oxygenase Modulates Prostate Cancer Growth via NF-κB Inhibition: A Lycopene-Independent Function

Gong

Raju²,

Zaripheh

et al. 2016

Molecular Cancer Research

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Despite numerous inquiries into protective roles of lycopene in prostate cancer prevention or therapy, little is known about mechanisms by which lycopene or its metabolites inhibit prostate cancer. The enzyme b-carotene 9',10'-oxygenase (BCO2), which catalyzes asymmetric cleavage of several carotenoids, is the principal regulator of lycopene metabolism, but the range of BCO2 biological functions is incompletely understood. This study investigated expression and functional roles of BCO2 in human prostate cancer. Expression of the bco2 gene is dramatically decreased in prostate cancer tissue and in a range of prostate cancer cell lines as compared with nonneoplastic prostate tissue and normal prostatic epithelial cells, respectively. Inhibition of DNA methyltransferase activity restored bco2 expression in prostate cancer cell lines tested. Treatment with lycopene or its metabolite, apo-10-lycopenal, also increased bco2 expression and reduced cell proliferation in androgen-sensitive cell lines, but lycopene neither altered bco2 expression nor cell growth in androgen-resistant cells. Notably, restoring bco2 expression in prostate cancer cells inhibited cell proliferation and colony formation, irrespective of lycopene exposure. Exogenous expression of either wild-type BCO2 or a mutant (enzymatically inactive) BCO2 in prostate cancer cells reduced NF-kB activity and decreased NF-kB nuclear translocation and DNA binding. Together, these results indicate epigenetic loss of BCO2 expression is associated with prostate cancer progression. Moreover, these findings describe previously unanticipated functions of BCO2 that are independent of its enzymatic role in lycopene metabolism.

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“…Some enter the blood associated with chylomicrons and both low-and high-density lipoproteins and are carried in the circulation to the tissues [Bendich and Olson, 1989;Lindqvist and Andersson, 2004]. Mammalian tissues, including human tissues, express both b-carotene-cleaving enzymes [Lindqvist and Andersson, 2004;von Lintig and Vogt, 2004;Lindqvist et al, 2005] suggesting that retinol synthesis can also occur locally at the tissue and organ level. Although both enzymes are expressed in many of the same tissues, significant differences exist.…”

Section: Discussionmentioning

confidence: 99%

The retinol signaling pathway in mouse pluripotent P19 cells

Chen¹,

Reese²

2011

J. Cell. Biochem.

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atRA (all-trans-retinoic acid), the active metabolite of retinol (vitamin A), is essential for embryogenesis and maintenance of cellular phenotype in adults. Chemicals that interfere with the metabolism of retinol to atRA, therefore, are a human health concern. During development of a screen for disruptors of this signaling pathway, we investigated whether the mouse pluripotent P19 cell metabolizes retinol to atRA and thus can be used in a cell-based screen for disruptors of the pathway. We found that retinol induced the identical pattern of homeobox gene expression as atRA and its precursor, retinal. Retinol was 160-fold less potent than atRA as an inducer, however. In spite of its lower potency, increased Hoxa1 gene expression was detected 30 min after retinol exposure and increased 40-fold by 2 h. Rdh10 and Aldh1a2/Raldh2, which together convert retinol to atRA in the embryo, were the predominant alcohol and aldehyde dehydrogenases expressed in P19 cells. The cell expressed high mRNA levels of retinol binding proteins, Rbp1 and Rbp4, and the 13,14-dihydroretinol saturase, Retsat. It also expressed all Rar and Rxr isotypes, Crabp1&2, the three Cyp26 genes, and both b-carotene-cleaving genes, Bcmo1 and Bco2. The basal expression levels and retinol responsiveness of 25 pathway-related genes were quantitated by RT-qPCR. A test of the Aldh1a2 inhibitor, citral, showed that the disruption of the pathway was easily detected and quantitated showing that the P19 cell provides an in vitro model system for identifying and exploring the mechanism of action of chemicals that interfere with this critical cellular pathway.

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Cell Type-specific Expression of β-Carotene 15,15′-Mono-oxygenase in Human Tissues

Cited by 73 publications

References 36 publications

Dietary carotenoids in normal and pathological tissues of corpus uteri.

Dietary carotenoids in normal and pathological tissues of corpus uteri.

Mitochondrial β-Carotene 9′,10′ Oxygenase Modulates Prostate Cancer Growth via NF-κB Inhibition: A Lycopene-Independent Function

The retinol signaling pathway in mouse pluripotent P19 cells

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