Helicobacter pylori Releases a Factor(s) Inhibiting Cell Cycle Progression of Human Gastric Cell Lines by Affecting Cyclin E/cdk2 Kinase Activity and Rb Protein Phosphorylation through Enhanced p27KIP1 Protein Expression

Sommi, Patrizia; Savio, Monica; Stivala, Lucia Anna; Scotti, Claudia; Mignosi, Paola; Prosperi, Ennio; Vannini, Vanio; Solcia, Enrico

doi:10.1006/excr.2002.5629

Cited by 30 publications

(26 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such analyses could also address whether there is any in vivo correlate to the observation from short term coculture that substances secreted by H pylori may also simultaneously increase the level of p27 protein expression. 49 In summary, our study supports a proapoptotic role for p27 in gastric cancer cells that is likely to explain, at least in part, the association of low levels of p27 with a poor prognosis in this disease. p27 and apoptosis resistance in gastric cells…”

Section: Discussionsupporting

confidence: 75%

p27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori

Eguchi

Carpentier

Kim

et al. 2004

Gut

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 75%

p27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori

Eguchi

Carpentier

Kim

et al. 2004

Gut

View full text Add to dashboard Cite

“…In previous work we have shown that H. pylori bacterial broth culture filtrate (BCF) can induce cell-cycle arrest (G1 phase) in several cell lines in a vacuolating cytotoxin A (VacA), cytotoxin-associated gene A (CagA) and Urease-independent manner [21]. This evidence suggested that one or more unknown bacterial factors could have an important role in this process and prompted us to pursue its/their isolation.…”

Section: Introductionmentioning

confidence: 99%

Cell-Cycle Inhibition by Helicobacter pylori L-Asparaginase

et al. 2010

View full text Add to dashboard Cite

Helicobacter pylori (H. pylori) is a major human pathogen causing chronic gastritis, peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue lymphoma. One of the mechanisms whereby it induces damage depends on its interference with proliferation of host tissues. We here describe the discovery of a novel bacterial factor able to inhibit the cell-cycle of exposed cells, both of gastric and non-gastric origin. An integrated approach was adopted to isolate and characterise the molecule from the bacterial culture filtrate produced in a protein-free medium: size-exclusion chromatography, non-reducing gel electrophoresis, mass spectrometry, mutant analysis, recombinant protein expression and enzymatic assays. L-asparaginase was identified as the factor responsible for cell-cycle inhibition of fibroblasts and gastric cell lines. Its effect on cell-cycle was confirmed by inhibitors, a knockout strain and the action of recombinant L-asparaginase on cell lines. Interference with cell-cycle in vitro depended on cell genotype and was related to the expression levels of the concurrent enzyme asparagine synthetase. Bacterial subcellular distribution of L-asparaginase was also analysed along with its immunogenicity. H. pylori L-asparaginase is a novel antigen that functions as a cell-cycle inhibitor of fibroblasts and gastric cell lines. We give evidence supporting a role in the pathogenesis of H. pylori-related diseases and discuss its potential diagnostic application.

show abstract

“…During the past decade, several bacterial effectors have been shown to interfere with p21 WAF1/CIP1 expression, such as the cyclomodulin cytolethal distending toxin from E. coli (63,64), toxin A from Clostridium difficile (65), or the CagA effector from Helicobacter pylori (66)(67)(68). Interestingly, the cycle inhibiting factor (Cif) produced by EPEC and EHEC bacteria differs from the toxins mentioned above in that Cif-induced accumulation of p21 WAF1/CIP1 does not involve transcription mechanisms but acts on a pathway controlling protein stability (69).…”

Section: Discussionmentioning

confidence: 99%

Disease and Carrier Isolates of Neisseria meningitidis Cause G ₁ Cell Cycle Arrest in Human Epithelial Cells

Papen¹,

Oosthuysen²,

Bécam³

et al. 2016

Infect Immun

View full text Add to dashboard Cite

Microbial pathogens have developed several mechanisms to modulate and interfere with host cell cycle progression. In this study, we analyzed the effect of the human pathogen Neisseria meningitidis on the cell cycle of epithelial cells. Two pathogenic isolates, as well as two carrier isolates, were tested for their ability to adhere to and invade into the epithelial cell lines Detroit 562 and NP69 and to modulate the cell cycle. We found that all isolates adhered equally well to both Detroit 562 and NP69 cells, whereas the carrier isolates were significantly less invasive. Using propidium iodide staining and 5-ethynyl-2=-deoxyuridine pulse-labeling, we provide evidence that meningococcal infection arrested cells in the G 1 phase of the cell cycle at 24 h postinfection. In parallel, a significant decrease of cells in the S phase was observed. Interestingly, G 1 -phase arrest was only induced after infection with live bacteria but not with heat-killed bacteria. By Western blotting we demonstrate that bacterial infection resulted in a decreased protein level of the cell cycle regulator cyclin D1, whereas cyclin E expression levels were increased. Furthermore, N. meningitidis infection induced an accumulation of the cyclin-dependent kinase inhibitor (CKI) p21 WAF1/CIP1 that was accompanied by a redistribution of this CKI to the cell nucleus, as shown by immunofluorescence analysis. Moreover, the p27 CIP1 CKI was redistributed and showed punctate foci in infected cells. In summary, we present data that N. meningitidis can interfere with the processes of host cell cycle regulation.

show abstract

Helicobacter pylori Releases a Factor(s) Inhibiting Cell Cycle Progression of Human Gastric Cell Lines by Affecting Cyclin E/cdk2 Kinase Activity and Rb Protein Phosphorylation through Enhanced p27KIP1 Protein Expression

Cited by 30 publications

References 35 publications

p27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori

p27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori

Cell-Cycle Inhibition by Helicobacter pylori L-Asparaginase

Disease and Carrier Isolates of Neisseria meningitidis Cause G ₁ Cell Cycle Arrest in Human Epithelial Cells

Contact Info

Product

Resources

About

Helicobacter pylori Releases a Factor(s) Inhibiting Cell Cycle Progression of Human Gastric Cell Lines by Affecting Cyclin E/cdk2 Kinase Activity and Rb Protein Phosphorylation through Enhanced p27KIP1 Protein Expression

Cited by 30 publications

References 35 publications

p27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori

p27kip1 regulates the apoptotic response of gastric epithelial cells to Helicobacter pylori

Cell-Cycle Inhibition by Helicobacter pylori L-Asparaginase

Disease and Carrier Isolates of Neisseria meningitidis Cause G 1 Cell Cycle Arrest in Human Epithelial Cells

Contact Info

Product

Resources

About

Disease and Carrier Isolates of Neisseria meningitidis Cause G ₁ Cell Cycle Arrest in Human Epithelial Cells