The Interferon Stimulated Gene 54 Promotes Apoptosis

Stawowczyk, Marcin; Scoy, Sarah Van; Kumar, K. Praveen; Reich, Nancy C.

doi:10.1074/jbc.m110.207068

Cited by 149 publications

(168 citation statements)

References 77 publications

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“…A number of IFN response genes have been linked to growth inhibition, senescence and apoptosis [49][50][51][52]. Our results suggest that under normal conditions, IFN-related genes are mostly repressed by the BRCA2 complex, and this repression is released in BRCA2 knockout cells.…”

Section: Discussionmentioning

confidence: 48%

Up-regulation of the interferon-related genes in BRCA2 knockout epithelial cells

Jian

Viré

et al. 2014

J. Pathol.

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BRCA2 mutations are significantly associated with early onset breast cancer, and the tumour suppressing function of BRCA2 has been attributed to its involvement in homologous recombination [1]-mediated DNA repair. In order to identify additional functions of BRCA2, we generated BRCA2-knockout HCT116 human colorectal carcinoma cells. Using genome-wide microarray analyses, we have discovered a link between the loss of BRCA2 and the up-regulation of a subset of interferon (IFN)-related genes, including APOBEC3F and APOBEC3G. The overexpression of IFN-related genes was confirmed in different human BRCA2 −/− and mouse Brca2 −/− tumour cell lines, and was independent of either senescence or apoptosis. In isogenic wild type BRCA2 cells, we observed over-expression of IFN-related genes after treatment with DNAdamaging agents, and following ionizing radiation. Cells with endogenous DNA damage because of defective BRCA1 or RAD51 also exhibited over-expression of IFN-related genes. Transcriptional activity of the IFN-stimulated response element (ISRE) was increased in BRCA2 The GEO number for microarray analysis is GSE54830. Author contributionsHX designed the study, carried out most experiments and wrote the manuscript. JX made the BRCA2 knockout cell lines in HCT116, performed DNA damage repair experiments on BRCA2 knockout cells and wrote part of the manuscript. EV performed the CHIP experiment and was involved in manuscript writing. SJ analyzed the data. JW carried out microarray analysis. RT and VW carried out experiments. TK, CC and SA were involved in study design.

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Section: Discussionmentioning

confidence: 48%

Up-regulation of the interferon-related genes in BRCA2 knockout epithelial cells

Jian

Viré

et al. 2014

J. Pathol.

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“…[13][14][15][16] IFIT2 regulates the functions of cell cycle, apoptosis, tumor colonization and viral replication, which confer cellular resistance to viral infections and regulates proliferation, apoptosis and migration of cancer cells. [17][18][19][20] In this report, we found that curcumin induced expression of interferon regulatory genes (especially IFIT2) in luekemia cell U937. upregulation of IFIT2 by exogenous expressing or treating with IFNg in K562 increased cells apoptosis and enhanced anticancer effect of curcumin.…”

Section: Introductionmentioning

confidence: 83%

“…IFIT2 has been demonstrated involved in anticancer process of other agents, but its role in the treatment of leukemia by curcumin still unknown. 26,27 Several researchers have shown that IFIT2 can induce apoptosis via a mitochondrial pathway dependent on Bcl ¡ 2 28,29 , and curcumin has been reported inducing apoptosis via BCL ¡ 2 signaling pathway as well. [30][31][32] The previous study suggested that BCR-ABL kinase domain inhibited the expression of ISRE-containing genes, 33 which could in part associated with resistant of K562.…”

Section: Discussionmentioning

confidence: 99%

Curcumin induces apoptosis in human leukemic cell lines through an IFIT2-dependent pathway

Zhang

Kong

Liu

et al. 2017

Cancer Biology & Therapy

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Curcumin, the primary bioactive component isolated from turmeric, has been shown to possess variety of biologic functions including anti-cancer activity. However, molecular mechanisms in different cancer cells are various. In the present study, we demonstrated that curcumin induced G2/M cell cycle arrest and apoptosis by increasing the expression levels of cleaved caspase-3, cleaved PARP and decreasing the expression of BCL ¡ 2 in U937 human leukemic cells but not in K562 cells. We found some interferon induced genes, especially interferon-induced protein with tetratricopeptide repeats 2 (IFIT2), were significantly upregulated when treated with curcumin in U937 cells by gene expression chip array, and further confirmed that the expression of IFIT2 was obviously higher in U937 than that in K562 cells by Western blot assay. In addition, inhibiting the expression of IFIT2 by shRNA in U937 rescued curcumininduced apoptosis and exogenous overexpression of IFIT2 by lentiviral transduction or treating with IFNg in K562 cells enhanced anti-cancer activity of curcumin. These results indicated for the first time that curcumin induced leukemic cell apoptosis via an IFIT2-dependent signaling pathways. The present study identified a novel mechanism underlying the antitumor effects of curcumin, and may provide a theoretical basis for curcumin combined with interferon in the cancer therapeutics.

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“…Clinically, these two interferons have been used with several success rates on the cases of keloid and burns [9]. Interferon can regulate the expression of genes related to apoptosis of fibroblast cell and sensitize several types of cell on the apoptosis stimuli, but the side effect limits the use of this therapy at last for prophylactic of scar and keloid [25], [26].…”

Section: Asian Journal Of Applied Sciences (Issn: 2321 -0893) Volume mentioning

confidence: 99%

The Role of L. plantarum as an Immunomodulator Secretion of Transforming Growth Factor-Î²1, Transforming Growth Factor-Î²3, and Interferon-Î± Macrophages and Dermal Fibroblasts

Shintawati

Sudigdoadi²,

Madjid³

et al. 2017

AJAS

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This research aims to see the effect of L.plantarum in modulating the secretion of Transforming Growth Factor-TGFÎ²1, TGFÎ²3 macrophages and fibroblasts, Interferon-IFNÎ± macrophages, and to analyze the possibility of L.plantarum potency in supporting the process of scarless wound healing. The culture of peritoneal macrophages was treated with L.plantarum for 24 hours, while another macrophage was S.aureus stimulated for 6 hours before treatment of L.plantarum for 24 hours. The formed supernatant was separated and centrifuged to serve as a treatment on the culture of rat dermal fibroblasts for 24 hours. The supernatant was then separated and centrifuged; its cytokine level was measured with enzyme-linked immunosorbent assay-ELISA. Treatment of L.plantarum with medium and high doses increased the secretion of IFNa macrophages compared with the control; all L.plantarum doses can stimulate the secretion of TGFÎ²1 fibroblast and TGFÎ²3 macrophage significantly, but it does not affect the secretion of TGFÎ²1 macrophages. It can be concluded that L.plantarum increased the secretion of IFNÎ± macrophages higher than the treatment preceded by S.aureus stimulation. The secretion of TGFÎ²1 fibroblasts and TGFÎ²3 fibroblasts also increased, but it was not as high as L.plantarum treatment stimulated by S.aureus. Therefore, the application of L.plantarum to support the process of wound healing, prophylactic of the excessive scar and fibrosis can be researched further.

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The Interferon Stimulated Gene 54 Promotes Apoptosis

Cited by 149 publications

References 77 publications

Up-regulation of the interferon-related genes in BRCA2 knockout epithelial cells

Up-regulation of the interferon-related genes in BRCA2 knockout epithelial cells

Curcumin induces apoptosis in human leukemic cell lines through an IFIT2-dependent pathway

The Role of <i>L. plantarum</i> as an Immunomodulator Secretion of <i>Transforming Growth Factor</i>-Î²1, <i>Transforming Growth Factor</i>-Î²3, and <i>Interferon</i>-Î± Macrophages and Dermal Fibroblasts

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