Expression of MicroRNA in Host Cells Infected with Helicobacter pylori
3
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
Background/Aims: MicroRNAs (miRNAs) regulate gene expression. We assess miRNA regulation by Helicobacter pylori infection and elucidate their role in H. pylori-infected gastric epithelial cells. Methods: The relationship between miRNA expression and DNA methylation was examined. Cells were treated with the nuclear factor-kappaB (NF-κB) inhibitor Bay 11-7082 to determine the relationship between miRNA expression and NF-κB signal transduction. Results: In the negative control cells infected with H. pylori 26695, the expression of six miRNAs was increased, whereas the expression of five miRNAs was decreased. The expression of upregulated miRNAs was increased when the host cells were treated with H. pylori and an NF-κB inhibitor. miR-127-5p, -155, and -181 were associated with increased interleukin 6 (IL-6) secretion in H. pylori infected cells treated with anti-miRNA. The expression of miR-155, -127-5p, -195, -216, -206, and -488 increased by approximately 3-fold following treatment with the methylation inhibitor Aza. Conclusions: We found novel miRNAs in H. pylori-infected negative control cells using miRNA microarrays. Upregulated miRNA expression was inversely related to the transcription of NF-κB. miR-195 and miR-488 appear to play a pivotal role in controlling IL-6 activity in H. pylori infection. miRNA expression in H. pylori infection was affected by methylation.
Abstract
Background/Aims: MicroRNAs (miRNAs) regulate gene expression. We assess miRNA regulation by Helicobacter pylori infection and elucidate their role in H. pylori-infected gastric epithelial cells. Methods: The relationship between miRNA expression and DNA methylation was examined. Cells were treated with the nuclear factor-kappaB (NF-κB) inhibitor Bay 11-7082 to determine the relationship between miRNA expression and NF-κB signal transduction. Results: In the negative control cells infected with H. pylori 26695, the expression of six miRNAs was increased, whereas the expression of five miRNAs was decreased. The expression of upregulated miRNAs was increased when the host cells were treated with H. pylori and an NF-κB inhibitor. miR-127-5p, -155, and -181 were associated with increased interleukin 6 (IL-6) secretion in H. pylori infected cells treated with anti-miRNA. The expression of miR-155, -127-5p, -195, -216, -206, and -488 increased by approximately 3-fold following treatment with the methylation inhibitor Aza. Conclusions: We found novel miRNAs in H. pylori-infected negative control cells using miRNA microarrays. Upregulated miRNA expression was inversely related to the transcription of NF-κB. miR-195 and miR-488 appear to play a pivotal role in controlling IL-6 activity in H. pylori infection. miRNA expression in H. pylori infection was affected by methylation.
참고문헌 (40)
- IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, "Schistosomes, liver flukes and Helicobacter pylori", pp.177~220 (1994), World Health Organization
- Yim JY, "Seroprevalence of Helicobacter pylori in South Korea", Helicobacter, 12, pp.333~340 (2007)
- Israel DA, "Helicobacter pylori genetic diversity within the gastric niche of a single human host", Proc Natl Acad Sci U S A, 98, pp.14625~14630 (2001)
- Nathan C, "Nonresolving inflammation", Cell, 140, pp.871~882 (2010)
- Khan MK, "Association of Helicobacter pylori infection and gastric carcinoma", Mymensingh Med J, 21, pp.80~84 (2012)
- Parsonnet J, "Helicobacter pylori and gastric cancer", Gastroenterol Clin North Am, 22, pp.89~104 (1993)
- Blaser MJ, "Helicobacter pylori persistence: biology and disease", J Clin Invest, 113, pp.321~333 (2004)
- Bartel DP, "MicroRNAs: target recognition and regulatory functions", Cell, 136, pp.215~233 (2009)
- Ambros V, "The functions of animal microRNAs", Nature, 431, pp.350~355 (2004)
- Okubo M, "Association between common genetic variants in pre-microRNAs and gastric cancer risk in Japanese population", Helicobacter, 15, pp.524~531 (2010)
- Bou Kheir T, "miR-449 inhibits cell proliferation and is down-regulated in gastric cancer", Mol Cancer, 10, pp.29~ (2011)
- Craig VJ, "Epigenetic silencing of microRNA-203 dysregulates ABL1 expression and drives Helicobacter-associated gastric lymphomagenesis", Cancer Res, 71, pp.3616~3624 (2011)
- Li N, "Increased miR-222 in H. pyloriassociated gastric cancer correlated with tumor progression by promoting cancer cell proliferation and targeting RECK", FEBS Lett, 586, pp.722~728 (2012)
- Saito Y, "Dysfunctional gastric emptying with down-regulation of muscle-specific microRNAs in Helicobacter pylori-infected mice", Gastroenterology, 140, pp.189~198 (2011)
- Lario S, "microRNA profiling in duodenal ulcer disease caused by Helicobacter pylori infection in a Western population", Clin Microbiol Infect, 18, pp.E273~E282 (2012)
- Belair C, "Helicobacter pylori interferes with an embryonic stem cell micro RNA cluster to block cell cycle progression", Silence, 2, pp.7~ (2011)
- Salama N, "A whole-genome microarray reveals genetic diversity among Helicobacter pylori strains", Proc Natl Acad Sci U S A, 97, pp.14668~14673 (2000)
- Zhu Y, "MicroRNAs up-regulated by CagA of Helicobacter pylori induce intestinal metaplasia of gastric epithelial cells", PLoS One, 7, pp.e35147~ (2012)
- Christman JK, "5-Azacytidine and 5-aza-2’-deoxycytidine as inhibitors of DNA methylation: mechanistic studies and their implications for cancer therapy", Oncogene, 21, pp.5483~5495 (2002)
- Yoshida M, "Potent and specific inhibition of mammalian histone deacetylase both in vivo and in vitro by trichostatin A", Tanpakushitsu Kakusan Koso, 52(13 Suppl), pp.1788~1789 (2007)
- Tsai KW, "Epigenetic regulation of miR- 34b and miR-129 expression in gastric cancer", Int J Cancer, 129, pp.2600~2610 (2011)
- Fassi Fehri L, "Helicobacter pylori induces miR-155 in T cells in a cAMP-Foxp3-dependent manner", PLoS One, 5, pp.e9500~ (2010)
- Xiao B, "Induction of microRNA-155 during Helicobacter pylori infection and its negative regulatory role in the inflammatory response", J Infect Dis, 200, pp.916~925 (2009)
- Oertli M, "MicroRNA- 155 is essential for the T cell-mediated control of Helicobacter pylori infection and for the induction of chronic gastritis and colitis", J Immunol, 187, pp.3578~3586 (2011)
- Liu Z, "Up-regulated microRNA-146a negatively modulate Helicobacter pylori-induced inflammatory response in human gastric epithelial cells", Microbes Infect, 12, pp.854~863 (2010)
- Li N, "H. pylori related proinflammatory cytokines contribute to the induction of miR-146a in human gastric epithelial cells", Mol Biol Rep, 39, pp.4655~4661 (2012)
- Gao C, "Reduced microRNA- 218 expression is associated with high nuclear factor kappa B activation in gastric cancer", Cancer, 116, pp.41~49 (2010)
- Feng Y, "FoxM1 is overexpressed in Helicobacter pylori-induced gastric carcinogenesis and is negatively regulated by miR-370", Mol Cancer Res, 11, pp.834~844 (2013)
- Ishimoto T, "Chronic inflammation with Helicobacter pylori infection is implicated in CD44 overexpression through miR-328 suppression in the gastric mucosa", J Gastroenterol, 50, pp.751~757 (2015)
- Akao Y, "let-7 microRNA functions as a potential growth suppressor in human colon cancer cells", Biol Pharm Bull, 29, pp.903~906 (2006)
- Yanaihara N, "Unique microRNA molecular profiles in lung cancer diagnosis and prognosis", Cancer Cell, 9, pp.189~198 (2006)
- Higashi H, "Biological activity of the Helicobacter pylori virulence factor CagA is determined by variation in the tyrosine phosphorylation sites", Proc Natl Acad Sci U S A, 99, pp.14428~14433 (2002)
- Azuma T, "Association between diversity in the Src homology 2 domain: containing tyrosine phosphatase binding site of Helicobacter pylori CagA protein and gastric atrophy and cancer", J Infect Dis, 189, pp.820~827 (2004)
- Brandt S, "NF-kappaB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein", Proc Natl Acad Sci U S A, 102, pp.9300~9305 (2005)
- Hayashi Y, "CagA mediates epigenetic regulation to attenuate let-7 expression in Helicobacter pylori-related carcinogenesis", Gut, 62, pp.1536~1546 (2013)
- Matsushima K, "MicroRNA signatures in Helicobacter pylori-infected gastric mucosa", Int J Cancer, 128, pp.361~370 (2011)
- Suzuki H, "Methylation-associated silencing of microRNA-34b", c in gastric cancer and its involvement in an epigenetic field defect, 2010, pp.31, 2066~2073
- Ando T, "DNA methylation of microRNA genes in gastric mucosae of gastric cancer patients: its possible involvement in the formation of epigenetic field defect", Int J Cancer, 124, pp.2367~2374 (2009)
- Shen J, "Epigenetic silencing of miR-490- 3p reactivates the chromatin remodeler SMARCD1 to promote Helicobacter pylori-induced gastric carcinogenesis", Cancer Res, 75, pp.754~765 (2015)
- Kiga K, "Epigenetic silencing of miR- 210 increases the proliferation of gastric epithelium during chronic Helicobacter pylori infection", Nat Commun, 5, pp.4497~ (2014)
