Modulation of Interferon (IFN)-inducible Gene Expression by Retinoic Acid

Kolla, Venkatadri; Lindner, Daniel J.; Xiao, Weihua; Borden, Ernest C.; Kalvakolanu, Dhananjaya V.

doi:10.1074/jbc.271.18.10508

Cited by 116 publications

(81 citation statements)

References 25 publications

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“…Taken together, these results show that RA is not able to induce directly tyrosine phosphorylation of Stat1. However, as shown previously in MCF-7, HL60 and WISH cells (Kolla et al, 1996;Pelicano et al, 1997), RA pretreatment of NB4 cells (more than one day) did signi®cantly increase Stat1 activation in response to IFNa or IFNg. In contrast, priming resistant cells for 3 days with RA had no e ect in increasing IFN responses in NB4-R1 and NB4-R2 cells; it may even cause a small decrease in Stat1 DNAbinding activity (Figure 4a).…”

Section: Stat1 Expression and Activation In Ra-treated Nb4 And Resistsupporting

confidence: 84%

“…We and others have also shown that RA impinges with the IFN system by upregulating the expression of the crucial transcription factors STAT (Stat1 and Stat2) and IRF (IRF-1 and p48) (Gianni et al, 1997;Kolla et al, 1996;Matikainen et al, 1996Matikainen et al, , 1997Pelicano and Chelbi-Alix, 1998;Pelicano et al, 1997). By upregulating Stat1 expression in IFN resistant breast tumour cells, RA is able to restore IFN sensitivity (Kolla et al, 1996).…”

Section: Discussionmentioning

confidence: 87%

“…By upregulating Stat1 expression in IFN resistant breast tumour cells, RA is able to restore IFN sensitivity (Kolla et al, 1996). It has been recently shown that RA increases the level of Stat1 and Stat2 in various cell lines (Gianni et al, 1997;Kolla et al, 1996;Matikainen et al, 1997;Pelicano and Chelbi-Alix, 1998;Pelicano et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Di erent studies have recently shown that RA directly increases the expression of three transcription factors playing a central role in the mechanisms of IFN action. RA increases the level of both STAT (Stat1 and Stat2) and IRF (IRF-1 and p48) gene expression (Gianni et al, 1997;Kolla et al, 1996;Matikainen et al, 1996Matikainen et al, , 1997Pelicano and Chelbi-Alix, 1998;Pelicano et al, 1997). Additional mechanisms could be involved as RA also causes the induction and secretion of IFN (Pelicano et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Retinoic acid resistance in NB4 APL cells is associated with lack of interferon α synthesis Stat1 and p48 induction

et al. 1999

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Section: Stat1 Expression and Activation In Ra-treated Nb4 And Resistsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Retinoic acid resistance in NB4 APL cells is associated with lack of interferon α synthesis Stat1 and p48 induction

et al. 1999

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“…RA regulates the growth and differentiation of many different cell types, and plays an important role in development (De Luca, 1991). Many genes are known to be modulated by RA treatment, such as Stra genes (Stra1 -13) (Bouillet et al, 1995;Boudjelal et al, 1997), midkine (Muramatsu et al, 1993), ICAM-1 (Cilenti et al, 1995), STAT1 (Kolla et al, 1996), IL-8 (Harant et al, 1996) and IL-2 receptor alpha subunit (Bhatti and Sidell, 1994). Among signal transduction molecules, c-erbB2 promoter activity and X17C (a novel MAP kinase phosphatase) were found to be upregulated by RA (Hudson et al, 1990;Mason et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Tyrosine-kinase expression profiles in human gastric cancer cell lines and their modulations with retinoic acids

et al. 2003

Br J Cancer

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Many protein tyrosine kinases are key regulators involved in cellular growth, differentiation, development, apoptosis and signal transduction pathways. Obtaining a comprehensive tyrosine-kinase expression profile in tumour cells is essential to learning more about their oncogenic potentials and responses to various chemotherapeutic reagents -such as retinoic acid, which has been shown to suppress the growth of gastric cancer cells and modulate gene expression. Expression of tyrosine kinases in retionic acid-treated cancer cells was investigated by reverse trancriptase -polymerase chain reaction (RT -PCR) and a novel restriction analysis of gene expression (RAGE) display technique. We first established comprehensive tyrosine-kinase profiles in different human gastric cancer cell lines. In cells treated with 9-cis-retinoic acid or all-trans-retinoic acid, we found that two PTKs (Eph and Hek5) appeared to be upregulated. In the present study, we demonstrate an efficient and simple RAGE approach for examining tyrosine kinases' expression in tumour cells and their alterations following drug treatments.

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All-trans Retinoic Acid Potentiates the Ability of Interferon Beta-1b to Augment Suppressor Cell Function in Multiple Sclerosis

Dayal²,

Jensen³

et al. 1998

Arch Neurol

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Treatment with interferon beta-1b partially restores defective T suppressor cell function in patients with MS. This potentially beneficial action is synergistically potentiated by RA. Interferon beta-1b increases the number of interferon gamma-secreting cells in the circulation when treatment is initiated. A similar increment in interferon gamma-secreting cells is observed when interferon beta-1b is added to cultural peripheral blood mononuclear cells in vitro. This potentially deleterious action of interferon beta-1b is reversed by RA. Interferon beta-1b inhibits lymphocyte proliferation modestly but reproducibly. This action of interferon beta-1b is unaltered by RA. These data provide a rationale for a trial of combination treatment with interferon beta-1b and RA in patients with MS.

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Modulation of Interferon (IFN)-inducible Gene Expression by Retinoic Acid

Cited by 116 publications

References 25 publications

Retinoic acid resistance in NB4 APL cells is associated with lack of interferon α synthesis Stat1 and p48 induction

Retinoic acid resistance in NB4 APL cells is associated with lack of interferon α synthesis Stat1 and p48 induction

Tyrosine-kinase expression profiles in human gastric cancer cell lines and their modulations with retinoic acids

All-trans Retinoic Acid Potentiates the Ability of Interferon Beta-1b to Augment Suppressor Cell Function in Multiple Sclerosis

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