Vitamin A, differentiation and cancer

Love, Jane M.; Gudas, Lorraine J.

doi:10.1016/0955-0674(94)90051-5

Cited by 139 publications

(99 citation statements)

References 49 publications

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“…3 Retinoic acids (RAs) are natural and synthetic derivatives of Vitamin A. Alltrans-retinoic acid and 9-cis-RA are active metabolites that bind and activate the nuclear receptors, all-trans-RA receptors (RARs) and retinoid X receptors (RXRs), and control expression of various genes. 4,5 RAs inhibit proliferation and induce differentiation of cancer cells. 6,7 Interestingly, RA and IFN potentiate each other to induce biological responses.…”

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confidence: 99%

Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-β and retinoic acid-induced cancer cell death

Huang

Chen

et al. 2006

Cell Death Differ

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Combination of retinoic acids (RAs) and interferons (IFNs) has synergistic apoptotic effects and is used in cancer treatment. However, the underlying mechanisms remain unknown. Here, we demonstrate that mitochondrial respiratory chain (MRC) plays an essential role in the IFN-b/RA-induced cancer cell death. We found that IFN-b/RA upregulates the expression of MRC complex subunits. Mitochondrial-nuclear translocation of these subunits was not observed, but overproduction of reactive oxygen species (ROS), which causes loss of mitochondrial function, was detected upon IFN-b/RA treatment. Knockdown of GRIM-19 (gene associated with retinoid-interferon-induced mortality-19) and NDUFS3 (NADH dehydrogenase (ubiquinone) Fe-S protein 3), two subunits of MRC complex I, by siRNA in two cancer cell lines conferred resistance to IFN-b/RA-induced apoptosis and reduced ROS production. In parallel, expression of late genes induced by IFN-b/RA that are directly involved in growth inhibition and cell death was also repressed in the knockdown cells. Our data suggest that the MRC regulates IFN-b/RA-induced cell death by modulating ROS production and late gene expression.

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confidence: 99%

Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-β and retinoic acid-induced cancer cell death

Huang

Chen

et al. 2006

Cell Death Differ

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“…Yet the exact mechanisms underlying the effectiveness of RA, especially its direct action on tumour cells, remain unclear. Retinoic acid binds to and induces the expression of retinoic acid receptors (RARs) and retinoid x receptors (RXRs), which activate gene expression to initiate the mechanisms that control cellular differentiation and cell growth (Love and Gudas, 1994). Treatment of cancer cells with RA is frequently accompanied by alterations of tumour cell surface proteins, including intercellular adhesion molecule (ICAM) (Triozzi et al, 1992; Bouillon and Audette, 1994).…”

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confidence: 99%

All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity

Chao¹,

Jiang²,

Shyu³

et al. 1997

Br J Cancer

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Summary All-trans retinoic acid (RA) was previously shown to regulate the growth of gastric cancer cells derived from the cell line SC-Mi. This study was designed to investigate the effect of RA on the sensitivity of SC-Mi cells to lymphokine-activated killer (LAK) activity. RA at the concentration range of 0.001-10 kM was shown to induce SC-Mi cells to exhibit resistance to LAK activity in a dose-dependent manner. A kinetics study indicated that a significantly increased resistance was detected after 2 days of co-culturing SC-Mi cells with RA and reached a maximum after 6 days of culture. Similar results were obtained from two other cancer cell lines: promyelocytic leukaemia HL-60 and hepatic cancer Hep 3B. A binding assay demonstrated that the binding efficacy between target SC-M1 cells and effector LAK cells was not altered by RA. Flow cytometric analyses revealed that RA exhibited no effect on the expression of cell surface molecules, including HLA class and class 11 antigens, intercellular adhesion molecule-1 and -2, and lymphocyte function antigen-3. Cell cycle analysis revealed that culture of SC-Mi cells with RA resulted in an increase in GJG, phase and a decrease in S phase, accompanied by a decrease in cyclin A and cyclin Bi mRNA as determined by Northern blot analysis. Additionally, RA was shown to enhance the expression of retinoic acid receptor a (RARa) in SC-Mi cells, and to have no effect on the expression of RARfi or RARy. Taken together, these results indicate that RA can significantly increase gastric cancer cells SC-Mi to resist LAK cytotoxicity by means of a cytostatic effect through a mechanism relating to cell cycle regulation. The prevailing ideas, such as a decrease in effector to target cell binding, a reduced MHC class antigen expression or an altered RARP expression, are not involved.

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“…RA, a metabolite of vitamin A, has a profound influence on cell growth, differentiation, and metabolism 31) . Prolonged deprivation of vitamin A in laboratory animals results in an increased incidence of spontaneous tumors, such as carcinomas.…”

Section: U343-g-asmentioning

confidence: 99%

GRIM-19 Expression and Function in Human Gliomas

Jin

Jung

Jin

et al. 2010

J Korean Neurosurg Soc

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Objective :We determined whether the expression of GRIM-19 is correlated with pathologic types and malignant grades in gliomas, and determined the function of GRIM-19 in human gliomas. Methods : Tumor tissues were isolated and frozen at -80˚C just after surgery. The tissues consisted of normal brain tissue (4), astrocytomas (2), anaplastic astrocytomas (2), oligodendrogliomas (13), anaplastic oligodendrogliomas (11), and glioblastomas (16). To profile tumor-related genes, we applied RNA differential display using a Genefishing TM DEG kit, and validated the tumor-related genes by reverse transcription polymerase chain reaction (RT-PCR). A human glioblastoma cell line (U343MG-A) was used for the GRIM-19 functional studies. The morphologic and cytoskeletal changes were examined via light and confocal microscopy. The migratory and invasive abilities were investigated by the simple scratch technique and Matrigel assay. The antiproliferative activity was determined by thiazolyl blue Tetrazolium bromide (MTT) assay and FACS analysis. Results : Based on RT-PCR analysis, the expression of GRIM-19 was higher in astrocytic tumors than oligodendroglial tumors. The expression of GRIM-19 was higher in high-grade tumors than low-grade tumors or normal brain tissue; glioblastomas showed the highest expression. After transfection of GRIM-19 into U343MG-A, the morphology of the sense-transfection cells became larger and more spindly. The antisensetransfection cells became smaller and rounder compared with wild type U343MG-A. The MTT assay showed that the sense-transfection cells were more sensitive to the combination of interferon-β and retinoic acid than U343MG-A cells or antisense-transfection cells; the antiproliferative activity was related to apoptosis.

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Vitamin A, differentiation and cancer

Cited by 139 publications

References 49 publications

Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-β and retinoic acid-induced cancer cell death

Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-β and retinoic acid-induced cancer cell death

All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity

GRIM-19 Expression and Function in Human Gliomas

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