Central role of interferon regulatory factor‐1 (IRF‐1) in controlling retinoic acid inducible gene‐I (RIG‐I) expression

Su, Zao-zhong; Sarkar, Devanand; Emdad, Luni; Barral, Paola M.; Fisher, Paul B.

doi:10.1002/jcp.21128

Cited by 62 publications

(67 citation statements)

References 51 publications

(60 reference statements)

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“…The expression of RIG-I without HVJ-E treatment was hardly detected in PC3 cells by western blot as seen in the previous report. 41 Thus, HVJ-E augments production of the cytoplasmic receptor of its RNA genome through the production of Type I IFN (Fig. 4b).…”

Section: Resultsmentioning

confidence: 94%

“…This is presumably because of the autocrine effect of secreted IFN as previously reported. 41 In fact, RIG-I was activated upon the addition of recombinant IFN to PC3 cells (data not shown), and the effect of HVJ-E on RIG-I up-regulation was abolished with use of an anti-IFN receptor antibody (Fig. 4b).…”

Section: Discussionmentioning

confidence: 90%

“…It is known that components of the viral genome must enter the cytoplasm because the cytoplasmic receptor, RIG-I helicase, must recognize doublestranded RNA of the Sendai virus genome to transmit a signal to IRF-3, which activates IFN transcription. 39,41 Therefore, tumor cell apoptosis appears to depend on the preferential binding of HVJ-E to hormone-resistant prostate cancer cells. The receptors of HVJ are GD1a and SPG.…”

Section: Discussionmentioning

confidence: 99%

“…mediated by both RIG-I and TLR-3. 39,41 With HVJ-E, membrane fusion occurs at the cell surface, not in endosomes. 22 The fact that gene delivery by HVJ-E is not affected by inhibitors of endocytosis 51,52 indicates that the viral genome can be directly delivered to the cytoplasm.…”

Section: Discussionmentioning

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: 94%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

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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“…Downstream signalling from RIG results in activation of NFκB and increased synthesis of Type I interferons. [15][16][17][18] The Path: How ATRA in Increased Type I Interferons…”

Section: Atramentioning

confidence: 99%

Potential for all-trans retinoic acid [tretinoin] to enhance interferon-alpha treatment response in chronic myelogenous leukemia, melanoma, myeloma, and renal cell carcinoma

Kast¹

2008

Cancer Biology & Therapy

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MicroRNA‐130b Ameliorates Murine Lupus Nephritis Through Targeting the Type I Interferon Pathway on Renal Mesangial Cells

Han

Wang

Zhang

et al. 2016

Arthritis & Rheumatology

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Objective. Type I interferon (IFN) is a critical pathogenic factor during the progression of lupus nephritis (LN). Although microRNAs (miRNAs) have been shown to control the IFN response in immune cells in LN, the role of miRNAs in resident renal cells remains unclear. We undertook this study to investigate the role of microRNA-130b (miR-130b) in the IFN pathway in renal cells as well as its therapeutic effect in LN.Methods. Kidney tissues from patients and (NZB 3 NZW)F1 lupus-prone mice were collected for detecting miR-130b levels. Primary renal mesangial cells (RMCs) were used to determine the role of miR-130b in the IFN pathway. We overexpressed miR-130b by administering miR-130b agomir in a mouse model of IFNa-accelerated LN to test its therapeutic efficacy.Results. Down-regulated miR-130b expression was observed in kidney tissues from patients and lupusprone mice. Further analysis showed that underexpression of miR-130b correlated negatively with abnormal activation of the IFN response in LN patients. In vitro, overexpressing miR-130b suppressed signaling downstream from the type I IFN pathway in RMCs by targeting IFN regulatory factor 1 (IRF-1). The opposite effect was observed when endogenous miR-130b expression was inhibited. The inverse correlation between IRF1 and miR-130b levels was detected in renal biopsy samples from LN patients. More importantly, in vivo administration of miR-130b agomir reduced IFNa-accelerated progression of LN, with decreased proteinuria, lower levels of immune complex deposition, and lack of glomerular lesions.Conclusion. MicroRNA-130b is a novel negative regulator of the type I IFN pathway in renal cells. Overexpression of miR-130b in vivo ameliorates IFNaaccelerated LN, providing potential novel strategies for therapeutic intervention in LN.Systemic lupus erythematosus (SLE) is a heterogeneous systemic autoimmune disease characterized by a wide range of clinical manifestations (1). Lupus nephritis (LN) is considered one of the most serious complications of SLE and the major indicator of a poor prognosis (2,3). The most common symptoms of LN are glomerular and tubulointerstitial inflammation, which

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Central role of interferon regulatory factor‐1 (IRF‐1) in controlling retinoic acid inducible gene‐I (RIG‐I) expression

Cited by 62 publications

References 51 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

Potential for all-trans retinoic acid [tretinoin] to enhance interferon-alpha treatment response in chronic myelogenous leukemia, melanoma, myeloma, and renal cell carcinoma

MicroRNA‐130b Ameliorates Murine Lupus Nephritis Through Targeting the Type I Interferon Pathway on Renal Mesangial Cells

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