Human glioma cells transformed by IGF-I triple helix technology show immune and apoptotic characteristics determining cell selection for gene therapy of glioblastoma

A, Ly; Ht, Duc; Kalamaridès, Michel; La, Trojan; Pan, Yinghong; Shevelev, Alexander; Jc, François; Noel, Tiffany; Kane, Ari J.; Hénin, Dominique; Dd, Anthony; Trojan, Jerzy

doi:10.1136/mp.54.4.230

Cited by 28 publications

(60 citation statements)

References 55 publications

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“…These observations help us to understand the regulation of MHC class I gene expression. Knowledge of the mechanisms involved in insulin/ IGF-I regulation of MHC class I transcription is important not only to understand the development of autoimmunity but also to find new strategies for cancer immunotherapy (Ly et al 2001, Yang & Meyskens 2005 …”

Section: Discussionmentioning

confidence: 99%

Transcriptional regulation of major histocompatibility complex class I gene by insulin and IGF-I in FRTL-5 thyroid cells

Giuliani¹,

Saji²,

Bucci³

et al. 2006

Journal of Endocrinology

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Increased major histocompatibility complex (MHC) class I gene expression in nonimmune cell 'target tissues' involved in organ-specific diseases may be important in the pathogenesis of autoimmune diseases. This possibility in part evolves from studies of cultured thyrocytes where properties appear relevant to the development of thyroid autoimmune disease. In FRTL-5 rat thyroid cells in continuous culture, hormones and growth factors that regulate cell growth and function specifically decrease MHC class I gene expression. We hypothesized that this could reflect a mechanism to preserve self-tolerance and prevent autoimmune disease. The mechanisms of action of some of these hormones, namely TSH and hydrocortisone, have been already characterized. In this report, we show that IGF-I transcriptionally downregulates MHC class I gene expression and that its action is similar to that of insulin. The two hormones have a complex effect on the promoter of the MHC class I gene, PD1. In fact, they decrease the full promoter activity, but upregulate the activity of deleted mutants that have lost an upstream, tissue-specific regulatory region but still retain the enhancer A region. We show that insulin/IGF-I promotes the interactions of the p50/p65 subunits of NF-B and AP-1 family members with these two regions, and that the tissue-specific region acts as a dominant silencer element on insulin/IGF-I regulation of promoter activity. These observations may be important to understand how MHC class I gene transcription is regulated in the cells.

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Section: Discussionmentioning

confidence: 99%

Transcriptional regulation of major histocompatibility complex class I gene by insulin and IGF-I in FRTL-5 thyroid cells

Giuliani¹,

Saji²,

Bucci³

et al. 2006

Journal of Endocrinology

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“…Immune response could be increased by different approaches as the injections of interferon, IL-2, activated lymphocytes, monoclonal antibodies or irradiated cells (i.e. Apuzzo & Mitchell, 1981) or using approach of IGF-I antisense treatment (Trojan et al, 1993;Ly et al, 2001). Previous results have shown that tumor cells of glioma, transfected with IGF-I antisense expression vector had no longer induced tumor formation, when injected into host recipients as compared to unmanipulated cells (Trojan et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…In the patients treated in the United States study, and in those investigated in Bromberg, Poland, tumour burden at time of treatment was advanced. One patient who was treated at University Hospitals of Cleveland, had lived 24 (Beckner et al, 2005;Fontenau et al, 2002;Ly et al, 2001;Trojan et al, 2007aTrojan et al, , 2010. Abréviations : TAP 1,2 (transporter associated with antigen processing antigen); TK (tyrosine kinase); PI3K (phosphatidyinositol 3 kinase); PDK1 (phosphoinositide-dependent kinase 1); AKT (PKB, protein kinase B); Bcl 2 (key molecule of apoptose); GSK3 (glycogene synthetase kinase 3); GS (glycogene synthetase); MAPK (MAP kinase -mitogen activated protein kinase); PKC (protein kinase C).…”

Section: Resultsmentioning

confidence: 99%

“…The IGF-I antisense transfected cells, when co-transfected with vectors encoding MHC-I and/or and B-7 antisense cDNA, however maintained their previous IGF-I « antisense » morphology, the number of apoptotic cells in the cultures of the double co-transfected IGF-I antisense glioma cells decreased from 60-70 to 20-30 % (Ly et al, 2001). The observation suggests that a relation could exist between immunogenicity and apoptosis in IGF-I transfected cells.…”

Section: Discussionmentioning

confidence: 99%

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Gene Therapy of Glioblastoma: Anti – Gene Anti IGF-I Strategy

Trojan¹

2011

Targets in Gene Therapy

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“…Les oligonucléotides antisens ont le même effet, ceci grâce à l'induction d'une ribonucléase spécifique, la RNase H [6,10,15,27]. Des ARN peuvent aussi être dirigés contre l'ADN de l'IGF-I ou de l'IGF-IR via la formation de triple hélice afin d'inhiber leur transcription [11,28].…”

Section: Les Arn Et Oligonucléotides Antisensunclassified

Thérapies antisens dirigées contre le récepteur de l’IGF-I

François

Trojan

2001

Med Sci (Paris)

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Human glioma cells transformed by IGF-I triple helix technology show immune and apoptotic characteristics determining cell selection for gene therapy of glioblastoma

Cited by 28 publications

References 55 publications

Transcriptional regulation of major histocompatibility complex class I gene by insulin and IGF-I in FRTL-5 thyroid cells

Transcriptional regulation of major histocompatibility complex class I gene by insulin and IGF-I in FRTL-5 thyroid cells

Gene Therapy of Glioblastoma: Anti – Gene Anti IGF-I Strategy

Thérapies antisens dirigées contre le récepteur de l’IGF-I

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