The Upregulation of <scp>TRAF</scp>1 Induced by <i>Helicobacter pylori</i> Plays an Antiapoptotic Effect on the Infected Cells

Wan, Xiukun; Yuan, Shengling; Tao, Hao-Xia; Diao, Li-Peng; Wang, Yanchun; Cao, Cheng; Liu, Chun‐Jen

doi:10.1111/hel.12311

Cited by 14 publications

(14 citation statements)

References 42 publications

(50 reference statements)

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“…There is no doubt that TRAF1 is an important factor for cancer progression. Many researchers have found that TRAF1 is upregulated in blood and solid tumors including stomach, ovarian, nasopharyngeal and skin cancers . TRAF1 is an important anti‐apoptotic factor in the NF‐κB and JNK pathways.…”

Section: Discussionmentioning

confidence: 99%

TNF receptor‐associated factor 1 as a biomarker for assessment of non‐small cell lung cancer metastasis and overall survival

Wen

Wang

Feng

et al. 2018

Clinical Respiratory J

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Our data showed that TRAF1 was significantly upregulated in NSCLC tissues. TRAF1 expression was positively associated with NSCLC lymphatic metastasis and clinical stage and was negatively associated with overall patient survival. TRAF1 promoted NSCLC cell proliferation CONCLUSION: TRAF1 expression was positively associated with NSCLC lymphatic metastasis and histological grade and was negatively associated with overall patient survival. TRAF1 may be an important therapeutic target for NSCLC.

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Section: Discussionmentioning

confidence: 99%

TNF receptor‐associated factor 1 as a biomarker for assessment of non‐small cell lung cancer metastasis and overall survival

Wen

Wang

Feng

et al. 2018

Clinical Respiratory J

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“…Previous research revealed that the expression of TRAF1 in response to H. pylori infection in gastric epithelial cells was mainly regulated by the activation of NF-kB. In addition, upregulation of TRAF1 plays an antiapoptotic role in H. pylori-infected gastric cells (50). Using the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, we found that TRAF1 also promoted anti-apoptosis activity via inducing the NF-κB signaling pathway.…”

Section: Discussionmentioning

confidence: 87%

Secretory leukocyte peptidase inhibitor expression and apoptosis effect in oral leukoplakia and oral squamous cell carcinoma

Wang

Jin

et al. 2018

Oncol Rep

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Oral leukoplakia (OL) is one of the most common oral precancerous lesions with the possibility of malignant transformation, ranging from 17 to 24% of patients with a median follow-up of >7 years. Previous research has revealed that compared with normal oral epithelial tissues, the expression of secretory leukocyte peptidase inhibitor (SLPI) protein is significantly reduced in oral squamous cell carcinoma (OSCC). Based on the above-mentioned research, it is known that SLPI is a potential predictive and diagnostic tool for the progression of oral carcinogenesis. Therefore, we investigated the correlation between the abundance of SLPI protein and the different histological grades of OL by immunohistochemistry. The results indicated that the level of SLPI was negatively correlated with the histological grades of the oral premalignant lesions, indicating that it may be a potential predictive tool for the malignant transformation presented in oral precancerous patients. Subsequently, we investigated the biological effects of SLPI using Cell Counting Kit (CCK)-8, Annexin V/PI apoptosis assay and Caspase-Glo® 3/7 assay. The findings revealed that SLPI promoted apoptosis in the Leuk1 and WSU-HN4 cell lines. Mechanistic studies indicated that SLPI, at least in part, regulated cell apoptosis by inhibiting the expression of TNF receptor-associated factor 1 (TRAF1), which has a close relationship with the nuclear factor-κB (NF-κB) pathway.

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“…The up-regulation of TRAF1 inhibited cell apoptosis and increased the viability of gastric epithelial cells infected with H. pylori . We also determined that H. pylori infection significantly enhanced the formation of the antiapoptotic complex containing TRAF1, TRAF2, cIAP1, and cIAP2, which might play a major role in suppressing the activation of caspase-8 and in inhibiting cell apoptosis[12]. …”

Section: Discussionmentioning

confidence: 99%

“…The up-regulation of TRAF1 inhibited cell apoptosis as well as increased the viability of infected cells, which suggested that TRAF1 is an important protein that contributes to the pathogenesis of H. pylori- related gastric cancer[12]. Interestingly, several studies have shown that TRAF1 could be transformed into a pro-apoptotic form after cleavage by caspase-8 in the presence of Fas ligand or TNF-α-induced apoptosis[13-15].…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori inhibits the cleavage of TRAF1 via a CagA-dependent mechanism

Wan¹,

Yuan²,

Wang³

et al. 2016

WJG

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AIMTo study the impact on cleavage of tumor necrosis factor receptor-associated factor 1 (TRAF1) regulated by Helicobacter pylori (H. pylori).METHODSCleavage of TRAF1 was detected by western blotting in the human gastric cancer cell line AGS following treatment with an apoptosis inducer. Cleavage of TRAF1 mediated by caspase was examined in vitro using specific caspase inhibitors. The effect of the COOH-terminal TRAF1 fragment on gastric cell apoptosis during H. pylori infection was measured using flow cytometry. The impact of H. pylori infection on TRAF1 cleavage was detected in the presence of apoptosis inducer. The roles of H. pylori virulence factors that may regulate TRAF1 cleavage were analyzed using isogenic cagA-, vacA- and cagE-null mutants.RESULTSTRAF1 was found to be cleaved in AGS cells treated with the apoptosis inducer, and caspase-8 was the major caspase involved in the cleavage of TRAF1. The COOH-terminal TRAF1 fragment significantly induced cell apoptosis (P < 0.05) as well as promoted H. pylori-induced cell apoptosis (P < 0.05). H. pylori infection was found to significantly inhibit the cleavage of TRAF1 and to inhibit the activation of caspase-8 in the presence of the apoptosis inducer at specific infection times and different cell/bacteria ratios. We also found that the effects of cagE- and cagA-null mutants on the inhibition of TRAF1 cleavage and activation of caspase-8 were significantly attenuated, compared with wild-type H. pylori, in the presence of the apoptosis inducer, showing that the virulence factor CagA was mainly involved in the inhibition of TRAF1 cleavage.CONCLUSIONH. pylori infection significantly inhibits the cleavage of TRAF1 via a CagA-dependent mechanism, which would increase the relative amounts of full-length TRAF1 and exert an antiapoptotic effect on H. pylori-infected cells.

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The Upregulation of TRAF1 Induced by Helicobacter pylori Plays an Antiapoptotic Effect on the Infected Cells

Abstract: H. pylori infection induces the overexpression of TRAF1 in gastric epithelial cells. The upregulation of TRAF1 plays an antiapoptotic role in H. pylori -infected gastric cells and may contribute to the gastric carcinogenesis.

Cited by 14 publications

References 42 publications

TNF receptor‐associated factor 1 as a biomarker for assessment of non‐small cell lung cancer metastasis and overall survival

TNF receptor‐associated factor 1 as a biomarker for assessment of non‐small cell lung cancer metastasis and overall survival

Secretory leukocyte peptidase inhibitor expression and apoptosis effect in oral leukoplakia and oral squamous cell carcinoma

Helicobacter pylori inhibits the cleavage of TRAF1 via a CagA-dependent mechanism

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