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Oncogene. 2003 Mar 20;22(11):1653-62.
Interferon-alpha sensitizes human hepatoma cells to TRAIL-induced apoptosis through DR5 upregulation and NF-kappa B inactivation.

Shigeno M, Nakao K, Ichikawa T, Suzuki K, Kawakami A, Abiru S, Miyazoe S, Nakagawa Y, Ishikawa H, Hamasaki K, Nakata K, Ishii N, Eguchi K.

First Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), a member of the TNF superfamily, induces apoptosis in a variety of cancer cells with little or no effect on normal cells. Human hepatoma cells, however, are resistant to TRAIL-induced apoptosis. Since interferon-alpha (IFN-alpha) is capable of enhancing TNF-alpha-induced apoptosis in certain cancer cells, we evaluated the effect of IFN-alpha on TRAIL-induced apoptosis of human hepatoma cells. IFN-alpha pretreatment enhanced TRAIL-induced apoptosis of HuH-7 and Hep3B cells, in which IFN-alpha upregulated the expression of DR5, a death receptor of TRAIL, and downregulated the expression of survivin, which has an antiapoptotic function. In contrast, IFN-alpha did not enhance TRAIL-induced apoptosis of HepG2 cells, in which expression of DR5 and survivin was not affected by IFN-alpha. On the other hand, TRAIL activated NF-kappa B composed of RelA-p50 heterodimer, a key transcription factor regulating cell survival, in HuH-7 and HepG2 cells. However, IFN-alpha pretreatment repressed the TRAIL-mediated activation of NF-kappaB and decreased its transcriptional activity in HuH-7 but not in HepG2 cells. Moreover, IFN-alpha pretreatment clearly augmented TRAIL-mediated caspase-8 activation in HuH-7 cells. Our results suggest that IFN-alpha could sensitize certain human hepatoma cells to TRAIL-induced apoptosis by stimulating its death signaling and by repressing the survival function in these cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12642868&dopt=Abstract

Leuk Res. 1999 Mar;23(3):255-61.
Establishment of a double Philadelphia chromosome-positive acute lymphoblastic leukemia-derived cell line, TMD5: effects of cytokines and differentiation inducers on growth of the cells.

Tohda S, Sakashita C, Fukuda T, Murakami N, Nara N.

Department of Laboratory Medicine, Tokyo Medical and Dental University, Japan.

A double Philadelphia chromosome (Ph)-positive leukemia cell line with common-B cell phenotype, designated TMD5, was established from the blast cells of a patient with double Ph-positive acute lymphoblastic leukemia. TMD5 cells expressed 190 kDa BCR/ABL chimeric protein and 145 kDa ABL protein. The cells proliferated without added growth factors. Autocrine growth mechanism was not recognized. The addition of growth factors such as G-CSF, GM-CSF, IL-3, IL-6, or Stem Cell Factor did not affect the growth. Herbimycin A suppressed the growth of TMD5 cells at the low concentration that did not affect Ph-negative cells. It suppressed tyrosine phosphorylation of intracellular proteins in TMD5 cells. Dexamethasone and dibutyryl cyclic AMP also suppressed the growth. They, however, did not affect the phosphorylation significantly. Neither all-trans retinoic acid nor interferon-alpha affected the growth. TMD5 cells, characterized minutely here and rare in that they have double Ph chromosomes, will be a useful tool for the study of Ph-positive leukemia.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10071078&dopt=Abstract

Neurosci Behav Physiol. 1999 Jan-Feb;29(1):37-44.
Systems analysis of the neuroimmunological mechanisms of memory.

Zhuravlev BV, Murtazina EP, Sulin VYu.

P. K. Anokhin Science Research Institute of Normal Physiology, Russian Academy of Medical Sciences, Moscow, Russia.

Experimental data on the role of immunomodulators in the mechanisms of neurological memory are presented and assessed from the point of view of functional systems theory. It is demonstrated that the immunomodulator interleukin-1 beta and the alpha-2-interferon fragment RITLY improve the processes of learning and reproduction of an active defensive habit. These substances were found to have effects on the productivity of behavior, on orientational-investigative reactions, and on vocalization in response to a conditioned signal. A positive correlation between intersignal activity and productivity is demonstrated as a reflection of the mechanisms of anticipatory reorganization of behavior during learning. However, interleukin has a selective action depending on the ethological conditions obtained during learning.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10088148&dopt=Abstract

Am J Physiol. 1999 Mar;276(3 Pt 1):G599-605.
Fas activates the JNK pathway in human colonic epithelial cells: lack of a direct role in apoptosis.

Abreu-Martin MT, Palladino AA, Faris M, Carramanzana NM, Nel AE, Targan SR.

Inflammatory Bowel Disease Center, Cedars-Sinai Medical Center, Los Angeles 90048, California, USA. abresmc.edu

Fas is expressed constitutively by colonic epithelial cells, and its ligand is expressed by intraepithelial and lamina propria lymphocytes. Fas ligation induces apoptosis in colonic epithelial cells and is implicated in the epithelial damage seen in ulcerative colitis. To understand the pleiotropic effects of Fas in the intestinal mucosa, we have examined signaling pathways activated by Fas in HT-29 colonic epithelial cells. HT-29 cells were stimulated with anti-Fas in the presence or absence of interferon-gamma (IFN-gamma). Activation of mitogen-activated protein kinase pathways was assessed by kinase assay, Western blots, and promoter-reporter assays. Electromobility shift assays were used to assess activator protein-1 (AP-1) binding activity. IFN-gamma increases expression of Fas on HT-29 cells. Signaling via Fas receptor, as determined by induction of c-Jun NH2-terminal kinase (JNK) activity and transcriptional activation of AP-1, is enhanced in IFN-gamma-primed cells. Dominant-interfering mutants of the JNK pathway do not block Fas-mediated apoptosis. Signaling through Fas results in activation of JNK and AP-1 binding activity that is increased in the presence of IFN-gamma. Inhibition of JNK does not block Fas-mediated apoptosis in these cells. Fas-Fas ligand interactions in the intestinal mucosa may lead to complex signal transduction cascades and gene regulation that culminate in apoptosis, cytokine secretion, or other novel functions.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10070035&dopt=Abstract

Immunogenetics. 1999 Apr;49(4):287-94.
Role of the interferon-stimulated response element in HLA-B downregulation in human melanoma cell lines.

Griffioen M, Ouwerkerk IJ, Harten V, Gobin SJ, van den Elsen PJ, Schrier PI.

Department of Clinical Oncology, Leiden University Medical Center, P. O. Box 9600, 2300 RC Leiden, The Netherlands.

Tumor cells are thought to escape immune surveillance from T cells by suppressing expression of major histocompatibility complex (MHC) class I molecules at their cell surface. Human MHC class I molecules are encoded by three different loci (HLA-A, -B, and -C). In primary human melanomas as well as melanoma cell lines, HLA class I expression is frequently downregulated in a B locus-specific manner. To study the involvement of promoter elements in HLA-B locus-specific downregulation, a series of reporter constructs containing 5'-flanking sequences of the HLA-A2 and -B7 genes were transfected into melanoma cell lines expressing high and low levels of HLA-B antigens. It is shown that enhancer A, which is generally believed to be a potent enhancer in HLA class I gene transcription, only weakly activates transcription in melanoma cell lines. In contrast, the interferon-stimulated response element (ISRE), known to induce MHC class I expression in response to IFNs, as well as a region comprising site alpha/enhancer B significantly stimulate constitutive transcription of HLA class I genes. Although none of the promoter elements tested could be demonstrated to mediate HLA-B locus-specific downregulation, high and low HLA-B melanoma cell lines do differ in ISRE activity as well as in ISRE-binding nuclear factors. The finding that high and low HLA-B melanoma cell lines contain different transcription factors binding to elements not actively involved in the process of HLA-B locus abrogation suggests that these cell lines originate from distinct types of melanocyte precursor cells expressing a different set of transcription factors.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10079292&dopt=Abstract

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