Antiproliferative Activity of the Human IFN-<i>α</i>-Inducible Protein IFI44

Hallen, Linda; Burki, Yvonne; Ebeling, Martin; Broger, Clemens; Siegrist, Fredy; Oroszlan-Szovik, Krisztina; Bohrmann, Bernd; Certa, Ulrich; Foser, Stefan

doi:10.1089/jir.2007.0021

Cited by 86 publications

(91 citation statements)

References 19 publications

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“…Microarray analysis revealed 17 IFN-induced genes (underlined) [33][34][35][36][37][38] among the 20 most up-regulated genes (Table I). This result suggests that the secretion of IFN by tumor cells following HVJ-E treatment might stimulate IFNrelated genes.…”

Section: Resultsmentioning

confidence: 99%

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Efficient eradication of hormone‐resistant human prostate cancers by inactivated Sendai virus particle

Kawaguchi

Miyamoto

Inoue

et al. 2009

Intl Journal of Cancer

138

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Hormone-refractory prostate cancer is one of the intractable human cancers in the world. Here, we examined the direct tumorkilling activity of inactivated Sendai virus particle [hemagglutinating virus of Japan envelope (HVJ-E)] through induction of Type I interferon (IFN) in the hormone-resistant human prostate cancer cell lines PC3 and DU145. Preferential binding of HVJ-E to PC3 and DU145 over hormone-sensitive prostate cancer cell and normal prostate epithelium was observed, resulting in a number of fused cells. After HVJ-E treatment, a number of IFNrelated genes were up-regulated, resulting in Type I IFN production in PC3 cells. Then, retinoic acid-inducible gene-I (RIG-I) helicase which activates Type I IFN expression after Sendai virus infection was up-regulated in cancer cells after HVJ-E treatment. Produced IFN-a and -b enhanced caspase 8 expression via Janus kinases/Signal Transducers and Activators of Transcription pathway, activated caspase 3 and induced apoptosis in cancer cells. When HVJ-E was directly injected into a mass of PC3 tumor cells in SCID (severe combined immunodeficiency) mice, a marked reduction in the bulk of each tumor mass was observed and 85% of the mice became tumor-free. Although co-injection of an antiasialo GM1 antibody with HVJ-E into each tumor mass slightly attenuated the tumor suppressive activity of HVJ-E, significant suppression of tumor growth was observed even in the presence of anti-asialo GM1 antibody. This suggests that natural killer cell activation made small contribution to tumor regression following HVJ-E treatment in hormone-resistant prostate cancer model in vivo. Thus, HVJ-E effectively targets hormone-resistant prostate cancer by inducing apoptosis in tumor cells, as well as activating anti-tumor immunity. '

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Section: Resultsmentioning

confidence: 99%

“…34 Interferon-induced protein 44 (IFI44) induces cell cycle-arrest. 35 Interferon induced transmembrane protein 1 (IFITM1) and interferon-induced protein with tetratricopeptide repeats 3 (IFIT3, also called RIG-G) are reported to generate anti-proliferation activity. 36,37 These 3 proteins presumably assist cancer cell death.…”

Section: Discussionmentioning

confidence: 99%

Efficient eradication of hormone‐resistant human prostate cancers by inactivated Sendai virus particle

Kawaguchi

Miyamoto

Inoue

et al. 2009

Intl Journal of Cancer

138

View full text Add to dashboard Cite

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“…SPINK4 (serine peptidase inhibitor Kazal type 4), which encodes a peptide structurally related to pancreatic secretory trypsin inhibitor, was reported as a candidate gene responsible for celiac disease (Wapenaar et al 2007). IFI44 (interferon-induced protein 44), which was originally identified to be a gene induced by interferon-a, has been suggested to encode an antiproliferative protein (Hallen et al 2007). …”

Section: Discussionmentioning

confidence: 99%

Identification of cis- and trans-acting factors involved in the localization of MALAT-1 noncoding RNA to nuclear speckles

Miyagawa

Tano

Mizuno

et al. 2012

RNA

216

192

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MALAT-1 noncoding RNA is localized to nuclear speckles despite its mRNA-like characteristics. Here, we report the identification of several key factors that promote the localization of MALAT-1 to nuclear speckles and also provide evidence that MALAT-1 is involved in the regulation of gene expression. Heterokaryon assays revealed that MALAT-1 does not shuttle between the nucleus and cytoplasm. RNAi-mediated repression of the nuclear speckle proteins, RNPS1, SRm160, or IBP160, which are well-known mRNA processing factors, resulted in the diffusion of MALAT-1 to the nucleoplasm. We demonstrated that MALAT-1 contains two distinct elements directing transcripts to nuclear speckles, which were also capable of binding to RNPS1 in vitro. Depletion of MALAT-1 represses the expression of several genes. Taken together, our results suggest that RNPS1, SRm160, and IBP160 contribute to the localization of MALAT-1 to nuclear speckles, where MALAT-1 could be involved in regulating gene expression.

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“…Among these were resistin like alpha and beta (Retnla and Retnlb) (Artis et al, 2004;Munitz et al, 2009;Wang et al, 2005), defensin beta 1 (Defb1) (Morrison et al, 2002), mast cell protease 9 (Mcpt9) (Friend et al, 1998), interferon-induced protein 44 (Ifi44) (Hallen et al, 2007), vav 1 oncogene (Vav1) (Spurrell et al, 2009), TBC1 domain family, member 23 (Tbc1d23) (De Arras et al, 2012) and several genes encoding 2′-5′ oligoadenylate synthetases (Oas1a, Oas1b, Oas1g, Oas2, Oas3) (Mashimo et al, 2003). Given that expression of Nkx2.2 is restricted to the intestinal epithelium, these gene expression changes are likely to be secondary to the dysregulation of enteroendocrine populations, such as cells expressing 5-HT, Cck and Ghrl, and support the emerging concept that enteroendocrine hormones can play immunomodulatory roles in the gut (Worthington, 2015).…”

Section: Characterization Of Nkx22mentioning

confidence: 99%

Lmx1a functions in intestinal serotonin-producing enterochromaffin cells downstream of Nkx2.2

et al. 2016

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Intestinal hormone-producing cells represent the largest endocrine system in the body, but remarkably little is known about enteroendocrine cell type specification in the embryo and adult. We analyzed stage-and cell type-specific deletions of Nkx2.2 and its functional domains in order to characterize its role in the development and maintenance of enteroendocrine cell lineages in the mouse duodenum and colon. Although Nkx2.2 regulates enteroendocrine cell specification in the duodenum at all stages examined, it controls the differentiation of progressively fewer enteroendocrine cell populations when deleted from Ngn3 + progenitor cells or in the adult duodenum. During embryonic development Nkx2.2 regulates all enteroendocrine cell types, except gastrin and preproglucagon. In developing Ngn3+ enteroendocrine progenitor cells, Nkx2.2 is not required for the specification of neuropeptide Y and vasoactive intestinal polypeptide, indicating that a subset of these cell populations derive from an Nkx2.2-independent lineage. In adult duodenum, Nkx2.2 becomes dispensable for cholecystokinin and secretin production. In all stages and Nkx2.2 mutant conditions, serotonin-producing enterochromaffin cells were the most severely reduced enteroendocrine lineage in the duodenum and colon. We determined that the transcription factor Lmx1a is expressed in enterochromaffin cells and functions downstream of Nkx2.2. Lmx1a-deficient mice have reduced expression of Tph1, the rate-limiting enzyme for serotonin biosynthesis. These data clarify the function of Nkx2.2 in the specification and homeostatic maintenance of enteroendocrine populations, and identify Lmx1a as a novel enterochromaffin cell marker that is also essential for the production of the serotonin biosynthetic enzyme Tph1.

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Antiproliferative Activity of the Human IFN-α-Inducible Protein IFI44

Cited by 86 publications

References 19 publications

Efficient eradication of hormone‐resistant human prostate cancers by inactivated Sendai virus particle

Efficient eradication of hormone‐resistant human prostate cancers by inactivated Sendai virus particle

Identification of cis- and trans-acting factors involved in the localization of MALAT-1 noncoding RNA to nuclear speckles

Lmx1a functions in intestinal serotonin-producing enterochromaffin cells downstream of Nkx2.2

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