Type III interferon induces apoptosis in human lung cancer cells

Li, Wei; Huang, Xi; Liu, Zhuoming; Wang, Yuxuan; Zhang, Hongwei; Tong, Hongfei; Wu, Hao; Lin, Sensen

doi:10.3892/or.2012.1901

Cited by 11 publications

(6 citation statements)

References 34 publications

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“…However, this result is somewhat different from the results of previous studies. In the previous studies, the expression of IFN λ1 in A549 cells was increased by the transfection of a plasmid expressing IFN λ1, and the proliferation of A549 cells was not affected (Li et al, ). In this study, IFN λ1 was added in the cell culture supernatant, and it affected the proliferation of A549 cells from two aspects, including apoptosis and autophagy, indicating that the route of administration of IFN λ1 might directly affect the therapeutic effect.…”

Section: Discussionmentioning

confidence: 92%

Role of autophagy in inhibiting the proliferation of A549 cells by type III interferon

Gao

Zhang

et al. 2019

Cell Biology International

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Interferons (IFNs) have anti‐viral and anti‐tumour effects. Type III interferon, as a member of the recently discovered interferon family, has been proved to inhibit tumour proliferation and promote the apoptosis of various tumour cells. However, whether type III IFN could inhibit the proliferation of lung cancer was not clear. In this study, we found that interferon λ (IFN λ) could inhibit the proliferation of A549 cells and induce autophagy and apoptosis of A549 cells. IFN λ could promote the expression of autophagy gene Beclin1 and interfere the expression of autophagy gene Beclin1 with small interfering RNA, thus inhibiting the effect of type III interferon on anti‐proliferation and promoting apoptosis of lung cancer cell. These results suggested that IFN λ could inhibit the proliferation of A549 cells by activating autophagy pathway, and IFN λ might be one of the potential therapeutic drugs for lung cancer.

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Section: Discussionmentioning

confidence: 92%

Role of autophagy in inhibiting the proliferation of A549 cells by type III interferon

Gao

Zhang

et al. 2019

Cell Biology International

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“…IFN-l and also IFN-b treatment induced the expression of KLF6, which would also lead to elevated TGF-b. Treatment with IFN-l causes cell cycle arrest in A549 (Li et al, 2012) and other cell lines (Li et al, 2008(Li et al, , 2010, and may do so via elevated TGF-b. The release of IFN-l during infection may also induce TGF-b expression and cell cycle arrest in neighbouring uninfected cells during RSV infection.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, induction of KLF6 by IFN-l/IFN-b but not LPS/polyI:C suggested that these cytokines could induce KLF6 expression via the Jak-Stat (Janus kinas-signal transducer and activator of transcription) pathway. Treatment with IFN-l does cause cell cycle arrest at G 0 /G 1 phase in A549 (Li et al, 2012) as well as other cell lines (Li et al, 2008(Li et al, , 2010.…”

Section: Rsv Ns1 Modulates Tgf-b Expression Via Klf6mentioning

confidence: 99%

Human respiratory syncytial virus non-structural protein NS1 modifies miR-24 expression via transforming growth factor-β

Bakre

Hiscox

et al. 2015

Journal of General Virology

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Human respiratory syncytial virus (RSV) is a major health challenge in the young and elderly owing to the lack of a safe and effective vaccine and proven antiviral drugs. Understanding the mechanisms by which viral genes and proteins modulate the host response to infection is critical for identifying novel disease intervention strategies. In this study, the RSV non-structural protein NS1 was shown to suppress miR-24 expression during infection. Lack of NS1 was linked to increased expression of miR-24, whilst NS1 overexpression suppressed miR-24 expression. NS1 was found to induce Kruppel-like factor 6 (KLF6), a transcription factor that positively regulates the transforming growth factor (TGF)-b pathway to induce cell cycle arrest. Silencing of KLF6 led to increased miR-24 expression via downregulation of TGF-b. Treatment with exogenous TGF-b suppressed miR-24 expression and induced KLF6. Confocal microscopy showed co-localization of KLF6 and RSV NS1. These findings indicated that RSV NS1 interacts with KLF6 and modulates miR-24 expression and TGF-b, which facilitates RSV replication. Received 23 March 2015Accepted 6 August 2015 INTRODUCTIONHuman respiratory syncytial virus (RSV) is a ubiquitous negative-sense ssRNA virus that can cause severe lung disease following infection (CDC, 2013;Hall et al., 2009;Nair et al., 2010). RSV is a member of the genus Pneumovirus, family Paramyxoviridae with a non-segmented genome that encodes 10 genes and 11 proteins (NS1, NS2, N, P, M, SH, G, F, M2-1, M2-2 and L). The two non-structural proteins (NS1 and NS2), which are not part of the intact virion, are transcribed and translated during infection (Moore et al., 2008).RSV infection rates are high and by age 2 years the majority of young children have experienced at least one infection (CDC, 2008(CDC, , 2013Hall et al., 2009;Mori et al., 2014;Nair et al., 2010;Stockman et al., 2012; Zhou et al., 2012). RSV infection in high-risk individuals, such as infants, young children, immunocompromised adults and the elderly, can manifest as serious pulmonary inflammatory disease including bronchiolitis and pneumonia (Hoffman et al., 2004;Moore et al., 2013;Openshaw & Chiu, 2013;Oshansky et al., 2009b;Psarras et al., 2004;Vicencio, 2010). There is also substantial evidence that early RSV infection can mediate airway remodelling, a feature that predisposes individuals to asthma development and exacerbation (Fong et al., 2000;Foronjy et al., 2014;Hirakawa et al., 2013;Hotard et al., 2015;Liesman et al., 2014;Meng et al., 2014;Piedimonte, 2002Piedimonte, , 2003Tan et al., 2008;Wu et al., 2011). Transforming growth factor (TGF)-b is expressed during RSV infection of lung epithelial cells (Gibbs et al., 2009;McCann & Imani, 2007;Mgbemena et al., 2011) and several studies indicate that it plays an important role in asthma development (de Faria et al., 2008;Fong et al., 2000;Gagliardo et al., 2013;Hoshino et al., 1998;Howell & McAnulty, 2006; Pelaia et al., 2007;Sharma et al., 2009). TGF-b also regulates aspects of the inflammatory cytokine r...

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“…IL28RA is widely present in various tissues of human body, and is highly expressed in organ tissues such as heart, bone marrow, pancreas, thyroid, skeletal muscle, prostate and testis [2] . Studies have shown that IFN-λs can activate JAK-STAT and PI3K/AKT signaling pathways to play antiviral, anti-tumor proliferation roles and regulate in ammatory responses [3][4][5][6][7][8] . IL28RA has has two alternative splicing (AS)variants, namely IL28RAVl and IL28RAV2, both of which can bind to type III interferon, but the latter loses the signal transduction function and can inhibit the activity of IFN-λs, so they have opposite functions [9] .…”

Section: Introductionmentioning

confidence: 99%

LncRNA260 siRNA promotes M2 macrophage polarization by reducing IL28RA alternative splicing

Yang

Gong

et al. 2022

Preprint

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Background and: Regulating the macrophages toward M2 polarization has become a therapeutic target for promoting cardiac repair after acute myocardial infarction (AMI). Macrophages can promote the transformation from inflammatory M1 type to anti-inflammatory M2 type by activating PI3K/AKT signaling pathway. In our previous study, we found that down-regulation of lncRNA260 could ameliorate hypoxic cardiomyocytes injury by regulating IL28RA through the activation of PI3K/AKT signaling pathways. It was suggested that lncRNA260 siRNA could promote the macrophages toward M2 polarization by regulating IL28RA. In this study, lncRNA260 siRNA was used to observe the polarization of mouse bone marrow macrophages and investigate its related mechanisms.Objective and methods: LncRNA 260 specific siRNA were designed and synthesized which were transfected into murine bone marrow-derived macrophages (BMDM)with liposomes. The experiment was divided into three groups: hypoxia group, hypoxia + lncRNA 260 specific siRNA transfection group, Normoxia group. The CD206-FITC/CD107b (Mac-3) or CD206-APC/CD11b-FITC double positive proportions were used to compare the M2 polarization ratio in the hypoxia process by using the immunofluorescence staining method. The p-AKT, Arginase 1, PI3KCG, IL28RAV1, IL28RAV2 proteins expression changes were observed by using the western blot method.Results: Compared with the Normoxia group, the double positive ratio of CD206-FITC/ Mac-3 and CD206-APC/CD11b-FITC were both significantly decreased in Hypoxia group (P<0.05). Compared with the hypoxia group, the double positive ratio of CD206-FITC/ Mac-3 and CD206/CD11b were both significantly increased in the Hypoxia + lncRNA260 siRNA transfection group (P<0.05). In the Hypoxia group, the ratios of Arg 1/β-Actin, p-AKT/β-Actin, PI3KCG/β-Actin, IL28RAV1/β-Actin were significantly lower than those in the Normoxia group (1.00±0.01) (P<0.05). After transfection with lncRNA260 siRNA, the ratios of Arg1/β-Actin, p-AKT/β-Actin , PI3KCG/β-Actin, IL28RAV1/β-Actin were significantly higher than those in the Hypoxia group (P<0.05) .Compared with the Normoxia group, the IL28RAV2/β-Actin in the Hypoxia group was significantly increased. After transfection with lncRNA260 siRNA, the ratio of IL28RAV2/β-Actin was significantly decreased than that in the Hypoxia group (P<0.05).Conclusion: LncRNA260 siRNA could promote the M2 polarization of the hypoxia macrophages by reducing the IL28RAV2 alternative splicing variant, which might be related to the activation of the JAK-STAT and PI3K/AKT signaling pathways.

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Type III interferon induces apoptosis in human lung cancer cells

Cited by 11 publications

References 34 publications

Role of autophagy in inhibiting the proliferation of A549 cells by type III interferon

Role of autophagy in inhibiting the proliferation of A549 cells by type III interferon

Human respiratory syncytial virus non-structural protein NS1 modifies miR-24 expression via transforming growth factor-β

LncRNA260 siRNA promotes M2 macrophage polarization by reducing IL28RA alternative splicing

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