Subcellular Accumulation of β-Carotene and Retinoids in Growth-Inhibited NCI-H69 Small Cell Lung Cancer Cells

Prakash, Pankaj; Jackson, Cynthia L.; Gerber, Leonard E.

doi:10.1207/s15327914nc340111

Cited by 16 publications

(7 citation statements)

References 21 publications

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“…However, it also suggests that CBP translocation to nucleus, under depleted GSH conditions, could also be facilitated by other mechanisms. Although, the precise mechanism for the transportation of CBP from cytosol to nucleus is not known, β-carotene and its breakdown products have been demonstrated to accumulate in crude nuclei of NCL-H69 cells46. Furthermore, the GSH supplementation significantly prevented the CBP-induced DNA damage in the ARPE-19 cells (Fig.…”

Section: Discussionmentioning

confidence: 94%

Genotoxic Effects of Carotenoid Breakdown Products in Human Retinal Pigment Epithelial Cells

Kalariya

Ramana

Srivastava

et al. 2009

Current Eye Research

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Purpose-To investigate the genotoxic effects of Lutein (LBP) & β-carotene breakdown products (β-apo-8-carotenal, BA8C) and preventive role of GSH in human retinal pigment epithelial cells (ARPE-19).Methods-LBP-and BA8C-induced DNA damage in human retinal pigment epithelial cells (ARPE-19) was determined by Comet assay. The DNA damage was quantified by the image analysis system using Comet Score™ software. ARPE-19 cell viability was determined by CellTiter 96 AQ ueous one solution cell proliferation assay kit. Intracellular GSH levels were measured by Ellman's reagent.

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Section: Discussionmentioning

confidence: 94%

Genotoxic Effects of Carotenoid Breakdown Products in Human Retinal Pigment Epithelial Cells

Kalariya

Ramana

Srivastava

et al. 2009

Current Eye Research

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“…It has been reported that β-carotene is primarily localized to the nuclei of NCI-H69 small lung cancer cells and plays a protective role by reducing their proliferation rate [35]. Though we did not analyze the nuclear fraction (P300× g) in these experiments, it is possible that a small fraction of BCO2 protein is localized to the nucleus upon treatment with β-carotene.…”

Section: Discussionmentioning

confidence: 96%

Palmitoylation of Metazoan Carotenoid Oxygenases

et al. 2020

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Abundant in nature, carotenoids are a class of fat-soluble pigments with a polyene tetraterpenoid structure. They possess antioxidant properties and their consumption leads to certain health benefits in humans. Carotenoid cleavage oxygenases (CCOs) are a superfamily of enzymes which oxidatively cleave carotenoids and they are present in all kingdoms of life. Complexity of CCO evolution is high. For example, in this study we serendipitously found a new family of eukaryotic CCOs, the apocarotenoid oxygenase-like (ACOL) family. This family has several members in animal genomes and lacks the animal-specific amino acid motif PDPCK. This motif is likely to be associated with palmitoylation of some animal CCOs. We recently demonstrated that two mammalian members of the carotenoid oxygenase family retinal pigment epithelial-specific 65 kDa protein (RPE65) and beta-carotene oxygenase 2 (BCO2) are palmitoylated proteins. Here we used the acyl-resin-assisted capture (acyl-RAC) method to demonstrate protein palmitoylation and immunochemistry to localize mouse BCO2 (mBCO2) in COS7 cell line in the absence and presence of its substrate β-carotene. We demonstrate that mBCO2 palmitoylation depends on the evolutionarily conserved motif PDPCK and that metazoan family members lacking the motif (Lancelet beta-carotene oxygenase-like protein (BCOL) and Acropora ACOL) are not palmitoylated. Additionally, we observed that the palmitoylation status of mBCO2 and its membrane association depend on the presence of its substrate β-carotene. Based on our results we conclude that most metazoan carotenoid oxygenases retain the evolutionarily conserved palmitoylation PDPCK motif to target proteins to internal membranes depending on substrate status. Exceptions are in the secreted BCOL subfamily and the strictly cytosolic ancient ACOL subfamily of carotenoid oxygenases.

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“…9 On the other hand, it is also possible that some of the effects induced by the carotenoid are due to its conversion to retinoic acid. ␤-Carotene cleavage to retinoic acid was demonstrated in some cultured cancer cells, such as small cell lung cancer cells 50 and colon adenocarcinoma cells. 51 However, it has been reported that several cancer cell lines, such as human breast, oral carcinoma and malignant melanoma, were not able to convert ␤-carotene to retinoic acid.…”

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confidence: 99%

Regulation of cell cycle progression and apoptosis by β‐carotene in undifferentiated and differentiated HL‐60 leukemia cells: Possible involvement of a redox mechanism

Palozza

Serini

Torsello

et al. 2001

Intl Journal of Cancer

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Although epidemiologic studies have demonstrated that a high intake of vegetables containing ␤-carotene lowers the risk of cancer, recent intervention studies have revealed that ␤-carotene supplementation to smokers resulted in a high incidence of lung cancer. We hypothesized that ␤-carotene may act as a pro-or anticancerogenic agent by modulating pathways involved in cell growth and that such a modulation may involve a redox mechanism. To test this hypothesis, cell proliferation, apoptosis and redox status were evaluated in undifferentiated and dimethylsulfoxide-differentiated HL-60 cells exposed to ␤-carotene. The carotenoid modified cell cycle progression and induced apoptosis in a dose-dependent manner. These effects were more remarkable in undifferentiated cells than in differentiated cells. In accord with these findings, in undifferentiated cells, ␤-carotene was more effective in decreasing cyclin A and Bcl-2 expression and in increasing p21 and p27 expression. Neither Bcl-xL nor Bax expression were significantly modified by the carotenoid. From a mechanistic point of view, the delay in cell growth by ␤-carotene was highly coincident with the increased intracellular reactive oxygen species production and oxidized glutathione content induced by the carotenoid. Moreover, ␣-tocopherol minimized the effects of ␤-carotene on cell growth. These data provide evidence that ␤-carotene modulates molecular pathways involved in cell cycle progression and apoptosis and support the hypothesis that a redox mechanism may be implicated. They also suggest that differentiated cells may be less susceptible to the carotenoid than highly neoplastic undifferentiated cells.

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Subcellular Accumulation of β-Carotene and Retinoids in Growth-Inhibited NCI-H69 Small Cell Lung Cancer Cells

Cited by 16 publications

References 21 publications

Genotoxic Effects of Carotenoid Breakdown Products in Human Retinal Pigment Epithelial Cells

Genotoxic Effects of Carotenoid Breakdown Products in Human Retinal Pigment Epithelial Cells

Palmitoylation of Metazoan Carotenoid Oxygenases

Regulation of cell cycle progression and apoptosis by β‐carotene in undifferentiated and differentiated HL‐60 leukemia cells: Possible involvement of a redox mechanism

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