Human papillomavirus 16E6 suppresses major histocompatibility complex class I by upregulating lymphotoxin expression in human cervical cancer cells

Kim, Donghern; Kim, Eun‐Mi; Lee, Eun-Hee; Ji, Kon-Young; Yi, Jawoon; Park, Min; Kim, Kwang Dong; Cho, Yong‐Yeon; Kang, Hyung‐Sik

doi:10.1016/j.bbrc.2011.05.090

Cited by 19 publications

(22 citation statements)

References 22 publications

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“…Moreover, HPV infection is often transient and the host immune system could counteract viral invasion leading to lesion regression [7], as the host immune system is able to counteract the infection. On the other hand, HPV is able to downregulate host immune system [8], blocking interferon response, antigen processing, and presentation [9] and modifying human leukocyte antigen (HLA)-G expression [10, 11]. …”

Section: Introductionmentioning

confidence: 99%

Infection and HLA-G Molecules in Nasal Polyposis

Rizzo

Mozzillo²,

Bortolotti

et al. 2014

Journal of Immunology Research

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Sinonasal polyposis (SNP) is a chronic inflammatory pathology with an unclear aetiopathogenesis. Human papillomavirus (HPV) infection is one candidate for the development of SNP for its epithelial cell trophism, hyperproliferative effect, and the induction of immune-modulatory molecules as HLA-G. We enrolled 10 patients with SNP without concomitant allergic diseases (SNP-WoAD), 10 patients with SNP and suffering from allergic diseases (SNP-WAD), and 10 control subjects who underwent rhinoplasty. We analyzed the presence of high- and low-risk HPV DNA and the expression of membrane HLA-G (mHLA-G) and IL-10 receptor (IL-10R) and of soluble HLA-G (sHLA-G) and IL-10 by polyp epithelial cells. The results showed the presence of HPV-11 in 50% of SNP-WoAD patients (OR:5.5), all characterized by a relapsing disease. HPV-11 infection was absent in nonrelapsing SNP-WoAD patients, in SNP-WAD patients and in controls, supporting the hypothesis that HPV-11 increases risk of relapsing disease. HPV-11 positive SNP-WoAD patients presented with mHLA-G and IL-10R on epithelial cells from nasal polyps and showed secretion of sHLA-G and IL-10 in culture supernatants. No HLA-G expression was observed in HPV negative polyps. These data highlight new aspects of polyposis aetiopathogenesis and suggest HPV-11 and HLA-G/IL-10 presence as prognostic markers in the follow-up of SNP-WoAD.

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Section: Introductionmentioning

confidence: 99%

Infection and HLA-G Molecules in Nasal Polyposis

Rizzo

Mozzillo²,

Bortolotti

et al. 2014

Journal of Immunology Research

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“…Due to these immune modulatory functions viruses may abuse LT-induced signaling pathways for their purposes. Human papillomavirus 16 E6 protein was recently proposed to induce LT and LTβR expression in cervical epithelial cell lines by downregulation of MHC class I molecules, thereby suppressing cytolytic antiviral responses [97]. Nevertheless, a clear demonstration of the underlying pathways is still lacking.…”

Section: Novel Effects Of Lt-mediated Signaling In Cancer Promotion Amentioning

confidence: 99%

Lymphotoxin, NF-ĸB, and Cancer: The Dark Side of Cytokines

Bauer

Namineni²,

Reisinger³

et al. 2012

Dig Dis

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Cytokines have been implicated in a variety of physiological processes involving lymphoid tissue development, lymphocyte activation, and control of regenerative processes such as wound healing. The first characterization of a cytokine implicated in abolishing or killing tumor cells – the tumor necrosis factor (TNF) – fostered and boosted a completely new field of research that in addition to cancer research started to generate an overwhelming amount of knowledge in immunology, various pathological processes, and other fields of research. Due to the complex networks and versatile functions of cytokines, it soon became clear that cytokines can possess diametric functions in various biological processes. As for tumor research it was shown that some cytokines – depending on the type of organ, the time of action, gender, and the cellular environment – can have either pro- or anticarcinogenic action. For those cytokines reported to be procarcinogenic, this could be accomplished by directly acting as oncogenes or generating an inflammatory environment that is procarcinogenic. Here we review a novel role for TNF family members – in particular lymphotoxin (LT) α and β – in physiology and in driving tumorigenesis, with special focus on the liver. We believe that recent findings on this particular cytokine might have strong implications for the therapy of liver cancer or other inflammation-induced cancer types.

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“…Total cytoplasmic RNA was isolated using TRIzol® reagent (MRC, Cincinnati, Ohio, USA), and the cDNAs were reverse transcribed with 5.0 μg of total RNA, 2.5 U of M-MLV reverse transcriptase (Promega, Madison, Wisc., USA) and 10 pmol of oligo(dT) primers at 42°C for 1 h. RT-PCR and real-time PCR were performed as described previously [14]. Primers used for RT-PCR were as follows: catalase (CAT), 5Ј-gcagatacctgtgaactgtc-3Ј and 5Ј-gtagaatgtccgcacctgag-3Ј; glutathione peroxidase (GPX), 5Ј-gcaatgtcgttgcggcacacc-3Ј and 5Ј-cctcaagtacgtccgacctg-3Ј; thioredoxin-1 (TRX-1), 5Ј-gtcgtggtggacttctctg-3Ј and 5Ј-gggtatagactctccacac-3Ј; peroxiredoxin-2 (PRX-2), 5Ј-agtaatggcctccggcaa-3Ј and 5Ј-tagcattttctgggccagca-3Ј, and β-actin, 5Ј-gacggccaggtcatcactat-3Ј and 5Ј-agtccgcctagaagcacttg-3Ј.…”

Section: Rt-pcr and Real-time Pcrmentioning

confidence: 99%

Interleukin-24 Suppresses the Growth of Vascular Smooth Muscle Cells by Inhibiting H<sub>2</sub>O<sub>2</sub>-Induced Reactive Oxygen Species Production

et al. 2012

Self Cite

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Background/Aim: The abnormal growth of vascular smooth muscle cells (VSMCs) induced by reactive oxygen species (ROS) is considered a major pathogenic process in vascular diseases. Interleukin (IL)-24 specifically inhibits cancer cell growth through the induction of cell cycle arrest and apoptosis. However, the role of IL-24 in ROS-induced VSMC growth has not yet been investigated. Methods: An MTT assay, gene expression analysis, flow cytometry and a scratch wound healing assay were performed to determine the anti-growth effects of IL-24 in H₂O₂-treated mouse vascular aortic smooth muscle (MOVAS) cells. To elucidate the effect of IL-24 on ROS-induced signaling, Western blot analysis was employed. Results: IL-24 inhibited the growth of normal MOVAS cells treated with H₂O₂ by inducing a cell cycle arrest at the G₀/G₁ phase through the regulation of p21 and cyclin D1. Furthermore, IL-24 suppressed mRNA expression of vascular endothelial growth factor and platelet-derived growth factor and subsequently decreased the level of cell migration in response to H₂O₂. Interestingly, IL-24 attenuated the H₂O₂-induced ROS production by reducing the mitochondrial H₂O₂ production and enhancing the expression of antioxidant enzymes. We also showed that the ability of H₂O₂ to induce the PI3K/Akt and Erk signaling pathways was blocked by IL-24. Conclusion: These findings suggest a novel mechanism in which IL-24 suppresses the growth of normal VSMCs by inhibiting H₂O₂-induced ROS production through the regulation of mitochondrial ROS production and expression of antioxidant enzymes.

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Human papillomavirus 16E6 suppresses major histocompatibility complex class I by upregulating lymphotoxin expression in human cervical cancer cells

Cited by 19 publications

References 22 publications

Infection and HLA-G Molecules in Nasal Polyposis

Infection and HLA-G Molecules in Nasal Polyposis

Lymphotoxin, NF-ĸB, and Cancer: The Dark Side of Cytokines

Interleukin-24 Suppresses the Growth of Vascular Smooth Muscle Cells by Inhibiting H<sub>2</sub>O<sub>2</sub>-Induced Reactive Oxygen Species Production

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