Helicobacter pylori inhibits gastric cell cycle progression

Helicobacterpylori-induced modification of the histone H3 phosphorylation status in gastric epithelial cells reflects its impact on cell cycle regulation

“…H. pylori is known to strongly affect the cell cycle of infected cells: G 1 /S and also G 2 /M cell cycle delays have been reported. [14][15][16][17][18] In our study, several observations point towards a strong contribution of an H. pylori-induced G 2 /M delay.…”

“…These findings are in accordance with other studies reporting H. pylori-induced G 1 /S and G 2 /M cell cycle delays. [14][15][16][17][18] Since the pH3Ser10 status is cell cycle-dependent, a new set of experiments was carried out using stricter cell cycle synchronization conditions, such as low serum starvation for 48 h and subsequent release with 10% FCS. In non-infected AGS cells, pH3Ser10 levels gradually increased with time (Suppl.…”

Late reactivation of sonic hedgehog by Helicobacter pylori results in population of gastric epithelial cells that are resistant to apoptosis: Implication for gastric carcinogenesis

“…However, most in vitro studies have shown the opposite result, that is, apoptosis prevails rather than proliferation after H. pylori or its supernatants treatment. Therefore, it is suggested that increased cell proliferation in gastric epithelium in vivo might be an indirect or secondary response to H. pylori infection [43][44][45]. Together with the previous publications that suppressed apoptosis might be one of major pathogenic factors in H. pylori-associated carcinogenesis [46][47][48] and oncogenic stem cells contributed to H. pylori-associated carcinogenesis [49], we could conclude that the reemergence of Shh expressing cells can explain these compensatory or counteractive privileges of proliferation through imbalanced epithelial turnover and this anti-apoptotic steps and proliferative privileges through Shh reactivation could be the necessary path for H. pylori-associated carcinogenesis.…”

Helicobacter pyloriinduces apoptosis of rat gastric parietal cells

“…Incubation may effectively alter the equilibrium between differentiation and apoptosis at a specific cellular signal-transduction step. Previous studies have revealed that H. pylori leads to a G1 arrest of a gastric epithelial cell line (1). H. pylori initiates epithelial cell signaling events that resulted in activation of the transcription factor NF-B (21).…”

“…Indeed, in vivo and in vitro studies demonstrate that infection with H. pylori is associated with apoptosis of gastric epithelial cells (20,31); coculture of human gastric cancer cell line (AGS) cells with H. pylori in vitro resulted in growth inhibition predominantly at the G(0)-G(1) checkpoint, possibly mediated by changes of the regulatory proteins p53, p21, and cyclin E (1). Another mechanism may be a more indirect effect.…”