Vitamin D receptor stable transfection restores the susceptibility to 1,25-dihydroxyvitamin D3cytotoxicity in a rat glioma resistant clone

Davoust, Nathalie; Wion, Didier; Chevalier, G.; Garabédian, M; Brachet, Philippe; Couez, Dominique

doi:10.1002/(sici)1097-4547(19980415)52:2<210::aid-jnr9>3.0.co;2-d

Cited by 29 publications

(20 citation statements)

References 34 publications

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“…Further four genes [namely, midkine (MDK), caspase 1 (CASP1), vitamin D receptor (VDR), and protein-L-isoaspartate O-methyltransferase (PCMT1)], for which the results were significantly correlated in our analyses (with MDK, CASP1 and VDR being positively correlated to TMZ resistance, and PCMT1 negatively correlated to TMZ resistance) (Fig. 2), have previously been reported to be associated with chemotherapy resistance, prognosis, tumor progression, or antiproliferation, in malignant gliomas (25)(26)(27)(28)(29).…”

Section: Resultsmentioning

confidence: 52%

“…However, again, none of these genes were identified in our microarray analysis. On the other hand, highly significant statistically positive-and negative-correlation of genes concerned with TMZ sensitivity/resistance were found as shown in Tables II and III (25)(26)(27)(28)(29), were differentially expressed in association with TMZ sensitivity/resistance in the glioma-derived cell lines. Among the genes positively correlated to TMZ resistance in our analysis, one of the most noteworthy is MGMT, as mentioned above; MGMT expression provides a resistance measure that can potentially be applied to current TMZ-based treatment strategies for malignant glioma patients.…”

Section: Discussionmentioning

confidence: 93%

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Gene expression profiling predicts response to temozolomide in malignant gliomas

Yoshino

Ogino²,

Yachi³

et al. 2010

Int J Oncol

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Abstract. Malignant gliomas are highly lethal neoplasms that cannot be cured with currently available therapies. Temozolomide (TMZ) is a recently introduced alkylating agent that has yielded significant benefits and become a key agent in the treatment of high-grade gliomas. However, its survival benefit remains unsatisfactory. Understanding the molecular basis of TMZ sensitivity/resistance is necessary for improving the treatment outcome by devising strategies that are able to circumvent primary drug resistance. We therefore combined the in vitro TMZ response with microarray gene expression data to identify genes that could potentially be used to predict the response of malignant gliomas to TMZ therapy. We first obtained the individual IC 50 values for TMZ in seven malignant glioma cell lines (A-172, AM-38, T98G, U-87MG, U-138MG, U-251MG and YH-13) and then identified the genes whose expression correlated most highly with TMZ sensitivity employing a cDNA microarray. We present here a list of the most highly up-regulated and down-regulated genes which may be involved in conferring TMZ sensitivity/resistance in malignant gliomas, although most of the genes have not been implicated as a causal factor in the TMZ response except MGMT. We also demonstrated and confirmed the MGMT methylation status, quantitative MGMT mRNA levels, and MGMT protein expression levels in TMZ resistant glioma cells in vitro. Our results are thus consistent with previous studies and suggest that a dominant mechanism conferring sensitivity/resistance to TMZ exists in malignant glioma cells. Although the present study dose have several limitations, our reported candidate genes could represent not only potential molecular markers for TMZ sensitivity/resistance but also chemotherapy targets. Furthermore, the present study could provide a foundation for alternative therapeutic strategies including novel combination treatments that incorporate additional reagents directed at overcoming resistance to TMZ.

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Section: Resultsmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 93%

Gene expression profiling predicts response to temozolomide in malignant gliomas

Yoshino

Ogino²,

Yachi³

et al. 2010

Int J Oncol

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“…As such, 1,25-(OH) 2 D 3 induced the cellular death of rat glioma cell lines [70][71][72] , and its in vitro efficacy was recently extended to human malignant cell lines [73][74][75][76] .…”

Section: Multiple Sclerosismentioning

confidence: 99%

Vitamin D and Ageing: Neurological Issues

et al. 2010

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nervous system as a whole, and in particular on the CNS. During cerebral development, vitamin D may act like a neurosteroid hormone in the areas of neurotrans mission, neuroprotection, and neuroimmunomodulation. Moreover, vitamin D deficiency has been associated with neurological and psychiatric disorders. In older adults, hypovitaminosis D has been associated with neuromuscular disorders, dementia, and Parkinson's disease. Thus, vitamin D supplementation might have a protective effect against these neurological disorders. Conclusions: Vitamin D has been associated with many neurological functions and its deficiency with dysfunction. Low serum 25-hydroxyvitamin D concentrations can potentially be reversed. This simple and low-cost correction might contribute to the primo-secondary prevention of various neuropsychiatric disorders.

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“…Vitamin D 3 is well known for its therapeutic activity against breast cancer, which in many cases requires the presence of functional VDR (9,10). Loss of VDR expression in human breast cancer cells is frequently associated with the resistance to vitamin D 3 -dependent growth inhibition (10), whereas its up-regulation by different means increases the sensitivity in different systems (11)(12)(13)(14). Alteration of VDR expression consequently emerges as an important approach for the regulation of vitamin D 3 activity in inhibition of cancer cell proliferation.…”

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confidence: 99%

The p38 and JNK Pathways Cooperate to trans-Activate Vitamin D Receptor via c-Jun/AP-1 and Sensitize Human Breast Cancer Cells to Vitamin D3-induced Growth Inhibition

Qi¹,

Pramanik²,

Wang³

et al. 2002

Journal of Biological Chemistry

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The signaling connection between mitogen-activated protein kinases(MAPKs) and nuclear steroid receptors is complex and remains mostly unexplored. Here we report that stress-activated protein kinases p38 and JNK trans-activate nuclear steroid vitamin D receptor ( p38 and c-Jun NH 2 -terminal kinase (JNK) 1 are the major MAPK pathways, which, together with the extracellular signalregulated kinase (ERK) pathways, convert signals of various extracellular stimuli into expression of specific target genes through phosphorylation and activation of transcription factors (1-3). The ERK pathway, downstream of Ras, is predominantly activated by mitogenic stimuli, whereas the p38 and JNK pathways are preferentially stimulated by environmental stresses. Although biological consequence of p38 and JNK activation in many cases overlaps with that of the ERK (1-3), one of its principle functions is regulation of stress and the inflammatory response (4, 5). The mechanisms leading to the functional diversity and/or specificity of the cellular physiological outcome of MAPK signaling are largely unknown and may relate to regulation of their specific downstream target genes. Although the p38 and JNK pathways can regulate expression of many molecules (2, 6), only a few of the true target genes selectively responsive to these stress pathways have been identified.The active form of vitamin D 3 , 1,25-dihydroxyvitamin D 3 , is a hormone with known activity in the regulation of calcium homeostasis, cell proliferation, and cell differentiation (7). Vitamin D 3 binds to its nuclear steroid receptor (VDR), a transcription factor, which dimerizes with itself or other nuclear receptors such as retinoid X receptor (RXR) to regulate gene expression by specific vitamin D response elements (VDREs) through which vitamin D 3 exerts its biological effects (7,8). Vitamin D 3 is well known for its therapeutic activity against breast cancer, which in many cases requires the presence of functional VDR (9, 10). Loss of VDR expression in human breast cancer cells is frequently associated with the resistance to vitamin D 3 -dependent growth inhibition (10), whereas its up-regulation by different means increases the sensitivity in different systems (11)(12)(13)(14). Alteration of VDR expression consequently emerges as an important approach for the regulation of vitamin D 3 activity in inhibition of cancer cell proliferation. The signaling mechanisms by which VDR is regulated, however, remain largely undiscovered.The signaling connection between MAPK activation and nuclear steroid hormone receptors is complex. The classical model is that the steroid hormone, because of its hydrophobic property, diffuses across the cellular membrane and binds to its nuclear receptor to regulate target gene expression through specific steroid receptor-responsive regulatory elements in the target genes, unrelated to MAPK regulation (15, 16). Recent experimental evidence suggests that there exist multiple interactions between the ERK-and JNK-MAPK pathways and the estrogen and proge...

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Vitamin D receptor stable transfection restores the susceptibility to 1,25-dihydroxyvitamin D3cytotoxicity in a rat glioma resistant clone

Cited by 29 publications

References 34 publications

Gene expression profiling predicts response to temozolomide in malignant gliomas

Gene expression profiling predicts response to temozolomide in malignant gliomas

Vitamin D and Ageing: Neurological Issues

The p38 and JNK Pathways Cooperate to trans-Activate Vitamin D Receptor via c-Jun/AP-1 and Sensitize Human Breast Cancer Cells to Vitamin D3-induced Growth Inhibition

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