CMTM3 protects the gastric epithelial cells from apoptosis and promotes IL-8 by stabilizing NEMO during Helicobacter pylori infection

Ning, Jing; Fu, Weiwei; Shi, Yanyan; Zhang, Jing; Ding, Shigang

doi:10.1186/s13099-023-00533-4

Cited by 5 publications

(4 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, we found that pretreatment, post-treatment, and cocultivation with ILA effectively mitigate the number of late apoptotic cells triggered by H. pylori (Figure D), thereby potentially contributing to the integrity of the gastric mucosa …”

Section: Resultsmentioning

confidence: 93%

“…Due to its induction of a reduction in gastric acid secretion and an increase in cell monolayer disintegration, apoptosis is advantageous for the establishment of H. pylori colonization and the disruption of local homeostasis. 31 Therefore, ILA also plays a protective role in preserving the integrity of gastric mucosal epithelial cells, thereby aiding resistance against invasion by H. pylori. The progression of H. pylori-induced gastric disease is typically accompanied by oxidative stress and inflammatory damage to the gastric mucosa.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, we found that pretreatment, post-treatment, and cocultivation with ILA effectively mitigate the number of late apoptotic cells triggered by H. pylori (Figure 4D), thereby potentially contributing to the integrity of the gastric mucosa. 31 Improvement of Gastric Tissue Abnormalities in Mice Induced by H. pylori Infection by ILA. We visually observed that mice infected with H. pylori exhibited abnormal gastric mucosa shape, along with damage and congestion compared to the group NC (Figure 5A).…”

Section: Effect Of Ila On Morphology Of H Pylorimentioning

confidence: 99%

See 2 more Smart Citations

Indole-3-Lactic Acid Derived from Lacticaseibacillus paracasei Inhibits Helicobacter pylori Infection via Destruction of Bacteria Cells, Protection of Gastric Mucosa Epithelial Cells, and Alleviation of Inflammation

Yao,

Cao,

Zhang

et al. 2024

J. Agric. Food Chem.

View full text Add to dashboard Cite

Indole-3-lactic acid (ILA) has exhibited antimicrobial properties. However, its role in inhibiting Helicobacter pylori infection remains elusive. This study investigated the inhibitory effect of ILA produced by Lacticaseibacillus paracasei on H. pylori, which was further confirmed by cell and animal experiments. 5 mg/mL ILA was sufficient to directly inhibit the growth of H. pylori in vitro, with a urease inhibitory activity reaching 60.94 ± 1.03%, and the cell morphology and structure were destroyed. ILA inhibited 56.5% adhesion of H. pylori to GES-1 and significantly reduced the number of apoptotic cells. Furthermore, ILA suppresses H. pylori colonization by approximately 38% to 63%, reduced inflammation and oxidative stress in H. pylori-infected mice, and enhanced the enrichment and variety of gut microbiota, notably fostering the growth of beneficial bacteria such as Lactobacillus and Bif idobacterium strains. The results support that ILA derived from Lactobacillus can be applicated as a novel prebiotic in anti-H. pylori functional foods.

show abstract

Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Effect Of Ila On Morphology Of H Pylorimentioning

confidence: 99%

See 1 more Smart Citation

Indole-3-Lactic Acid Derived from Lacticaseibacillus paracasei Inhibits Helicobacter pylori Infection via Destruction of Bacteria Cells, Protection of Gastric Mucosa Epithelial Cells, and Alleviation of Inflammation

Yao,

Cao,

Zhang

et al. 2024

J. Agric. Food Chem.

View full text Add to dashboard Cite

show abstract

“…The H. pylori -cell co-culture experiment was carried out as described previously. 61 , 62 Briefly, H. pylori collected from the solid medium was washed and resuspended in phosphate buffered saline (PBS). The quantity of H. pylori was measured at 600 nm absorbance using a spectrophotometer.…”

Section: Methodsmentioning

confidence: 99%

AUF1-mediated inhibition of autophagic lysosomal degradation contributes to CagA stability and Helicobacter pylori -induced inflammation

Zheng,

Zhang,

Zhang

et al. 2024

Gut Microbes

Self Cite

View full text Add to dashboard Cite

CagA, a virulence factor of Helicobacter pylori ( H. pylori ), is known to drive inflammation in gastric epithelial cells and is typically degraded through autophagy. However, the molecular mechanism by which CagA evades autophagy-mediated degradation remains elusive. This study found that H. pylori inhibits autophagic flux by upregulating the expression of AU-rich element RNA-binding factor 1 (AUF1). We confirmed that AUF1 does not affect autophagy initiation but instead hampers lysosomal clearance, as evidenced by treatments with 3-MA, CQ and BafA1. Upregulated AUF1 stabilizes CagA protein levels by inhibiting the autolysosomal degradation of intracellular CagA in H. pylori -infected gastric epithelial cells. Knocking down AUF1 promotes CagA degradation, an effect that can be reversed by the lysosome inhibitor BafA1 and CQ. Transcriptome analysis of AUF1-knockdown gastric epithelial cells infected with H. pylori indicated that AUF1 regulates the expression of lysosomal-associated hydrolase genes, specifically CTSD, to inhibit autolysosomal degradation. Moreover, we observed that knockdown of AUF1 enhanced the stability of CTSD mRNA and identified AUF1 binding to the 3’UTR region of CTSD mRNA. AUF1-mediated downregulation of CTSD expression contributes to CagA stability, and AUF1 overexpression leads to an increase in CagA levels in exosomes, thus promoting extracellular inflammation. In clinical gastric mucosa, the expression of AUF1 and its cytoplasmic translocation are associated with H. pylori -associated gastritis, with CagA being necessary for the translocation of AUF1 into the cytoplasm. Our findings suggest that AUF1 is a novel host-positive regulator of CagA, and dysregulation of AUF1 expression increases the risk of H. pylori -associated gastritis.

show abstract

CMTM6 promotes hepatocellular carcinoma invasion and metastasis and tumor-associated neutrophil immunoinfiltration through the Wnt/β-catenin pathway

Kong,

Yang,

Liu

et al. 2024

Eur J Med Res

View full text Add to dashboard Cite

Background CMTM6 has been closely associated with the onset and progression of various tumor types. However, the precise mechanism by which CMTM6 operates in hepatocellular carcinoma remains elusive, necessitating further investigation. Methods Expression levels of CMTM6 in hepatocellular carcinoma tissues and cells were analyzed using immunohistochemistry and quantitative real-time PCR. The correlation between CMTM6 expression in hepatocellular carcinoma tissues and clinical pathological characteristics, as well as patient prognosis, was investigated. Proliferation and apoptosis of hepatocellular carcinoma cells with silenced or overexpressed CMTM6 were assessed, alongside measurements of β-catenin and Wnt1 protein expression levels. In vivo research was conducted utilizing a murine subcutaneous transplantation model. Gene Set Enrichment Analysis (GSEA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed to elucidate the regulatory mechanism of CMTM6. Additionally, CD66b expression levels in tumor tissue were examined using immunohistochemistry, and the immune infiltration of CMTM6 and tumor-associated neutrophils (TANs) was analyzed. Results Elevated expression levels of CMTM6 in hepatocellular carcinoma tissues and cells were found to be associated with poor patient prognosis. Overexpression of CMTM6 in hepatocellular carcinoma cells was demonstrated to promote cellular proliferation and inhibit apoptosis. Mechanistically, CMTM6 expression levels in hepatocellular carcinoma tissues were observed to positively correlate with β-catenin expression. GSEA and KEGG analysis revealed significant enrichment of CMTM6 in the Wnt/β-catenin pathway, indicating its involvement in pathway regulation. Furthermore, CMTM6 was found to be associated with immune infiltration of TANs in hepatocellular carcinoma tissues. Conclusion CMTM6 plays a pivotal role in the development and progression of hepatocellular carcinoma through regulation of the Wnt/β-catenin pathway via β-catenin. Moreover, CMTM6 demonstrates the capacity to promote immune infiltration of TANs in hepatocellular carcinoma tissues. Consequently, CMTM6 exhibits potential as both an early diagnostic marker and a novel therapeutic target for patients with hepatocellular carcinoma. Supplementary Information The online version contains supplementary material available at 10.1186/s40001-024-02189-5.

show abstract

CMTM3 protects the gastric epithelial cells from apoptosis and promotes IL-8 by stabilizing NEMO during Helicobacter pylori infection

Cited by 5 publications

References 61 publications

Indole-3-Lactic Acid Derived from Lacticaseibacillus paracasei Inhibits Helicobacter pylori Infection via Destruction of Bacteria Cells, Protection of Gastric Mucosa Epithelial Cells, and Alleviation of Inflammation

Indole-3-Lactic Acid Derived from Lacticaseibacillus paracasei Inhibits Helicobacter pylori Infection via Destruction of Bacteria Cells, Protection of Gastric Mucosa Epithelial Cells, and Alleviation of Inflammation

AUF1-mediated inhibition of autophagic lysosomal degradation contributes to CagA stability and Helicobacter pylori -induced inflammation

CMTM6 promotes hepatocellular carcinoma invasion and metastasis and tumor-associated neutrophil immunoinfiltration through the Wnt/β-catenin pathway

Contact Info

Product

Resources

About