<i>Helicobacter pylori</i>‐downregulated tumor necrosis factor receptor‐associated protein 1 mediates apoptosis of human gastric epithelial cells

Teng, Yong‐Sheng; Liu, Xin; Han, Bin; Ma, Qiang; Liu, Yugang; Kong, Hui; Lv, Yi-pin; Mao, Fang‐Yuan; Cheng, Ping; Hao, Chuan-jie; Yang, Shi‐Ming; Zhang, Jinyu; Li, Peng; Zou, Quanming; Zhuang, Yuan

doi:10.1002/jcp.28223

Cited by 7 publications

(3 citation statements)

References 31 publications

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“…In addition, TRAP1 may regulate the malignant biology of cells by increasing the expression of CyclinB1, CyclinD1, CyclinE, MMP-2, and VEGF, leading to the development and progression of gastric cancer, which is an important target for targeted therapy. H. pylori vacuolating cytotoxin A (vacA) is involved in the regulation of apoptosis in human gastric epithelial cells by inducing down-regulation of TRAP1 via the P38MAPK pathway ( 147 ). In esophageal cancer (EC) TE-1 cells, shikonin promotes apoptosis and attenuates migration and invasion through inhibition of TRAP1 expression and AKT/mTOR signaling, suggesting that shikonin may be a novel drug for the treatment of EC ( 148 ).…”

Section: Mthsp90 Inhibitors In Cancersmentioning

confidence: 99%

The development of cancers research based on mitochondrial heat shock protein 90

Xiang,

Liu,

Sun

et al. 2023

Front. Oncol.

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Mitochondrial heat shock protein 90 (mtHsp90), including Tumor necrosis factor receptor-associated protein 1 (TRAP1) and Hsp90 translocated from cytoplasm, modulating cellular metabolism and signaling pathways by altering the conformation, activity, and stability of numerous client proteins, and is highly expressed in tumors. mtHsp90 inhibition results in the destabilization and eventual degradation of its client proteins, leading to interference with various tumor-related pathways and efficient control of cancer cell development. Among these compounds, gamitrinib, a specific mtHsp90 inhibitor, has demonstrated its safety and efficacy in several preclinical investigations and is currently undergoing evaluation in clinical trials. This review aims to provide a comprehensive overview of the present knowledge pertaining to mtHsp90, encompassing its structure and function. Moreover, our main emphasis is on the development of mtHsp90 inhibitors for various cancer therapies, to present a thorough overview of the recent pre-clinical and clinical advancements in this field.

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Section: Mthsp90 Inhibitors In Cancersmentioning

confidence: 99%

The development of cancers research based on mitochondrial heat shock protein 90

Xiang,

Liu,

Sun

et al. 2023

Front. Oncol.

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“…A multiplicity of infection (MOI) of 100 was used in cell infection. The relative bacterial number was determined by measuring OD at 600 nm (1OD 600 = 1 3 10 9 CFU/ml) (33).…”

Section: H Pylori Strains and Infectionmentioning

confidence: 99%

Helicobacter pylori CagA Interacts with SHP-1 to Suppress the Immune Response by Targeting TRAF6 for K63-Linked Ubiquitination

Liu

et al. 2021

The Journal of Immunology

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Helicobacter pylori is the major etiological agent for most gastric cancer. CagA has been reported to be an important virulence factor of H. pylori, but its effect on the immune response is not yet clear. In this study, wild-type C57BL/6 mice and Ptpn6me-v/me-v mice were randomly assigned for infection with H. pylori. We demonstrated that CagA suppressed H. pylori–stimulated expression of proinflammatory cytokines in vivo. Besides, we infected mouse peritoneal macrophages RAW264.7 and AGS with H. pylori. Our results showed that CagA suppressed expression of proinflammatory cytokines through inhibiting the MAPKs and NF-κB pathways activation in vitro. Mechanistically, we found that CagA interacted with the host cellular tyrosine phosphatase SHP-1, which facilitated the recruitment of SHP-1 to TRAF6 and inhibited the K63-linked ubiquitination of TRAF6, which obstructed the transmission of signal downstream. Taken together, these findings reveal a previously unknown mechanism by which CagA negatively regulates the posttranslational modification of TRAF6 in innate antibacterial immune response and provide molecular basis for new therapeutics to treat microbial infection.

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“…The isolation of human primary GECs (EpCAM + ) from tissues were performed as previously described 34 . Human primary GECs and AGS (ATCC) were cultured with DME/F12 (AGS) or RPMI 1640 (Human primary GECs) medium supplemented with 10% fetal bovine serum (FBS) at 37°C in 5% CO 2 .…”

Section: Cell Culture and Stimulationmentioning

confidence: 99%

Expression of ETS1 in gastric epithelial cells positively regulate inflammatory response in Helicobacter pylori-associated gastritis

Teng

Cang²,

Mao

et al. 2020

Cell Death Dis

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Gastric epithelial cells (GECs) provide the first point of contact of the host by Helicobacter pylori (H. pylori), and the interaction between H. pylori and GECs plays a critical role in H. pylori-associated diseases. Aberrant expression of transcription factors (TFs) contributes to the pathogenesis of inflammatory disorders, including H. pylori-associated gastritis. ETS (E26 transformation specific) transcription factor family is one of the largest families of evolutionarily conserved TFs, regulating critical functions during cell homeostasis. We screened ETS family gene expression in H. pylori-infected mouse and human GECs and found that ETS1 (ETS proto-oncogene 1, transcription factor) expression was highly affected by H. pylori infection. Then, we reported that ETS1 was induced in GECs by H. pylori via cagA activated NF-κB pathway. Notably, we demonstrated that proinflammatory cytokines IL-1β and TNFα have synergistic effects on ETS1 expression during H. pylori infection in an NF-κB-pathway-dependent manner. RNA-seq assay and Gene-ontology functional analysis revealed that ETS1 positively regulate inflammatory response during H. pylori infection. Increased ETS1 is also detected in the gastric mucosa of mice and patients with H. pylori infection. Collectively, these data showed that ETS1 may play an important role in the pathogenesis of H. pylori-associated gastritis.

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Helicobacter pylori‐downregulated tumor necrosis factor receptor‐associated protein 1 mediates apoptosis of human gastric epithelial cells

Cited by 7 publications

References 31 publications

The development of cancers research based on mitochondrial heat shock protein 90

The development of cancers research based on mitochondrial heat shock protein 90

Helicobacter pylori CagA Interacts with SHP-1 to Suppress the Immune Response by Targeting TRAF6 for K63-Linked Ubiquitination

Expression of ETS1 in gastric epithelial cells positively regulate inflammatory response in Helicobacter pylori-associated gastritis

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