Helicobacter pylori-induced gastric inflammation and gastric cancer

Wang, Fei; Meng, Wenbo; Wang, Bingyuan; Qiao, Liang

doi:10.1016/j.canlet.2013.08.016

Cited by 648 publications

(500 citation statements)

References 70 publications

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“…The activation of NF-kB and upregulation of IL8 in gastric epithelial cells have been suggested as critical mechanisms responsible for H. pylori-induced chronic inflammation and gastric carcinogenesis (47). The expression of most cancer biomarkers is driven by NF-kB-regulated genes (48).…”

Section: Discussionmentioning

confidence: 99%

Uncontrolled Inflammation Induced by AEG-1 Promotes Gastric Cancer and Poor Prognosis

Zhao

et al. 2014

Cancer Research

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Gastric cancer is one of the most common causes of cancer-related death worldwide. Helicobacter pylori infection plays an important role in the development and progression of gastric cancer. The expression of astrocyte-elevated gene-1 (AEG-1) is increased in gastric cancer tissues, thereby contributing to the inflammatory response. We investigated whether and how AEG-1 regulated proinflammatory signaling in gastric cancer cells. We used human gastric cancer cell lines and athymic nude mice to investigate the role of AEG-1 in the regulation of the TLR4/nuclear factor-kB (NF-kB) signaling pathway and cancer invasion and compared the expression of AEG-1 and related proteins in 93 patients with gastric cancer by immunohistochemistry. In human gastric cancer cells, both AEG-1 and TLR4 could be induced by lipopolysaccharide (LPS) stimulation. AEG-1 was upregulated via LPS-TLR4 signaling and in turn promoted nuclear translocation of the NF-kB p65 subunit. At the same time, AEG-1 overexpression decreased the levels of suppressor of cytokine signaling (SOCS) protein SOCS-1, a negative regulator of the TLR4 pathway. Furthermore, nude mice engrafted with AEG-1/TLR4-expressing cells demonstrated larger tumor volumes than control animals. In patients with gastric cancer, the expression of AEG-1 correlated with that of TLR4, SOCS-1, and NF-kB and was higher in tumors compared with noncancerous adjacent tissues. Overall survival in patients with gastric cancer with simultaneous expression of AEG-1 and TLR4 was poor. Our results demonstrate that AEG-1 can promote gastric cancer progression by a positive feedback TLR4/NF-kB signaling-related mechanism, thus providing new mechanistic explanation for the role of inflammation in cancer progression. Cancer Res; 74(19);

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Section: Discussionmentioning

confidence: 99%

Uncontrolled Inflammation Induced by AEG-1 Promotes Gastric Cancer and Poor Prognosis

Zhao

et al. 2014

Cancer Research

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“…Multiple risk factors have been identified to be involved in the initiation and progression of gastric cancer, including old age, smoking, alcohol consumption, obesity, unhealthy diet, low economic status, pernicious anemia, other chronic gastric diseases and Helicobacter pylori infection (3,4). The current comprehensive care strategy for gastric cancer is a combination of surgery, chemotherapy and radiotherapy (5).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑139 inhibits the proliferation, migration and invasion of gastric cancer cells by directly targeting ρ‑associated protein kinase 1

et al. 2018

Oncol Lett

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Abstract. The expression, function and underlying mechanisms of microRNA-139 (miR-139) in gastric cancer were investigated in the present study. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect miR-139 expression in gastric cancer tissues and cell lines. The effects of miR-139 overexpression on gastric cancer cell proliferation, migration and invasion were evaluated. ρ-associated protein kinase 1 (ROCK1) was predicted as a downstream target of miR-139 and its role in gastric cancer was assessed by bioinformatics analysis, luciferase reporter assay, RT-qPCR and western blot analysis. ROCK1 overexpression was established to investigate if the effects of miR-139 on gastric cancer cells may be attenuated. The results indicated that miR-139 was aberrantly downregulated in gastric cancer tissues and cell lines. Increased miR-139 expression reduced gastric cancer cell proliferation, migration and invasion. ROCK1 was demonstrated to be a direct target of miR-139 in gastric cancer and ROCK1 overexpression reversed the suppressive effects on gastric cancer cell proliferation, migration and invasion induced by miR-139 overexpression. The present study provides clear evidence demonstrating the anti-oncogenic activity of miR-139 in human gastric cancer, as mediated by the targeted downregulation of ROCK1.

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“…El Helicobacter pylori es una bacteria bacilar gramnegativa que habita en la mucosa gástrica, se asocia con enfermedades gastrointestinales inflamatorias como úlcera pép-tica, gastritis crónica y neoplásicas como los linfomas tipo MALT (tejido linfoide asociado a mucosas) donde la producción de citotoxinas como la asociada al gen A (cagA) y la vacuolizante (vacA) han sido asociados (1,2). H. pylori se adquiere durante la niñez, permanece de forma asintomática durante muchos años y el contacto cercano es un factor de riesgo (3,4).…”

Section: Introductionunclassified

Susceptibilidad antibiótica de Helicobacter pylori: un estudio de prevalencia en pacientes con dispepsia en Quito-Ecuador

Reyes

Guzmán

Morales

et al. 2017

Rev. Colomb. Gastroenterol.

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Introducción: Helicobacter pylori se lo asocia a patologías gastro-intestinales, el incremento en la resistencia a los antibióticos utilizados para su erradicación es alarmante a nivel mundial. En este estudio se determinó la susceptibilidad a cinco antibióticos utilizados en la terapia de erradicación de H. pylori aislado de una población adulta con dispepsia recurrente en Quito-Ecuador.Materiales y métodos: Previa aceptación del consentimiento informado, se tomaron biopsias de cuerpo y fondo gástrico de 210 pacientes con dispepsia, mediante cultivo se recuperaron los aislados de H. pylori identificado mediante pruebas bioquímicas. La susceptibilidad al metronidazol, claritromicina, amoxicilina, tetraciclina y levofloxacina se realizó por concentración mínima inhibitoria (CMI). Todos los cultivos se correlacionaron con el estudio histopatológico.Resultados: Se recuperaron 89 aislados de H. pylori. Se obtuvo un kappa de 0.9 entre el cultivo y el estudio histopatológico. El porcentaje de cepas con resistencia antibiótica fue: metronidazol (63 %), claritromicina (66 %), amoxicilina (43%), tetraciclina (36%) y levofloxacina (54%).Conclusión: Estos hallazgos demuestran la alta resistencia a los antibióticos usados para la erradicación de H. pylori, varios factores como consumo indiscriminado de antibióticos, terapia previa, etc. podrían estar involucrados.Palabras clave: Helicobacter pylori; resistencia antibiótica; concentración mínima inhibitoria.

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Helicobacter pylori-induced gastric inflammation and gastric cancer

Cited by 648 publications

References 70 publications

Uncontrolled Inflammation Induced by AEG-1 Promotes Gastric Cancer and Poor Prognosis

Uncontrolled Inflammation Induced by AEG-1 Promotes Gastric Cancer and Poor Prognosis

MicroRNA‑139 inhibits the proliferation, migration and invasion of gastric cancer cells by directly targeting ρ‑associated protein kinase 1

Susceptibilidad antibiótica de Helicobacter pylori: un estudio de prevalencia en pacientes con dispepsia en Quito-Ecuador

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