Epigenetic changes in gastric cancer induction by Helicobacter pylori

Abstract

Epigenetic disorder mechanisms are one of the causes of cancer. The most important of these changes is the DNA methylation, which leads to the spread of Helicobacter pylori and inflammatory processes followed by induction of DNA methylation disorder.Mutations and epigenetic changes are the two main agents of neoplasia. Epithelial cells infection byH. pylori associated with activating several intracellular pathways including: MAPK, NF-κB, Wnt/β-catenin, and PI3K are affects a variety of cells and caused to an increase in the production of inflammatory cytokines, changes in apoptosis, proliferation, differentiation, and ultimately leads to the transformation of epithelial cells into oncogenic. The arose of free radicals impose the DNA cytosine methylation, and NO can increase the activity of DNA methyltransferase. H. pylori infection causes an environment that mediates inflammation and signaling pathways that probably caused to stomach tumorigenicity. The main processes that change by decreasing or increasing the expression of various microRNAs expressions include immune responses, apoptosis, cell cycle, and autophagy. In this review will be describe a probably H. pylori roles in infection and mechanisms that have contribution in epigenetic changes in the promoter of genes. K E Y W O R D S epigenetic, gastric cancer, Helicobacter pylori, methylation, miRNAs

Factors Influencing Epigenetic Mechanisms: Is There A Role for Bariatric Surgery?

“…Aberrant methylation of gastric mucosal genes is a common finding in humans infected with Helicobacter pylori and is an early event in gastric carcinogenesis [21]. The change in the epigenetic profile in response to infection may play a role in the development of related immune disorders and tumors previously associated with infectious agents [22]. Importantly, some epigenetic modifications acquired during pregnancy can be transmitted from generation to generation, though fertilization usually removes DNA methylation.…”

Association of Helicobacter pylori vacA genotypes and peptic ulcer in Iranian population: a systematic review and meta-analysis

“…H. pylori and NSAIDs by independent mechanisms, but synergistically lead to severe in ammation and consequently peptic ulcer (12)(13). H. pylori is a microaerophilic, S shaped, gram negative, and motile (by lophotrichous agella) bacterium which is able to be colonized in human stomach (14). Almost half of world population are infected to H. pylori, nevertheless, the rate of colonization in developing countries is more compared to western countries; most of population in developing countries rst time infected with this bacterium in childhood ages (14)(15).…”

“…H. pylori is a microaerophilic, S shaped, gram negative, and motile (by lophotrichous agella) bacterium which is able to be colonized in human stomach (14). Almost half of world population are infected to H. pylori, nevertheless, the rate of colonization in developing countries is more compared to western countries; most of population in developing countries rst time infected with this bacterium in childhood ages (14)(15). The International Agency for Research on Cancer (IARC) introduced this bacterium as the main causing enemy of gastric cancer (15)(16).…”

“…These variable sequences are found in different regions from N-terminal side including signal sequence (s1 and s2) region, intermediate (i1 and i2) region, deletion (d1 and d2) region, and mid (m1 and m2) region, respectively. Whilst the cytotoxicity power of all genotypes differs from each other, in addition, two s1 and m1 regions in turn comprise several subtypes including s1a, s1b, s1c, m1a, m1b and m1c (14,(18)(19)(20). This antigen through induction of cytoplasmic vacuolation and apoptosis in infected cells can lead to the death of host gastric epithelial cells (14,21).…”

“…Whilst the cytotoxicity power of all genotypes differs from each other, in addition, two s1 and m1 regions in turn comprise several subtypes including s1a, s1b, s1c, m1a, m1b and m1c (14,(18)(19)(20). This antigen through induction of cytoplasmic vacuolation and apoptosis in infected cells can lead to the death of host gastric epithelial cells (14,21). In addition, the toxin causes dysregulation of normal signaling pathway via happens such as alternation in the mitogen-activated protein kinases (MAPKs) pathway, polarization, suppression of proliferation and migration, as well as cytoskeletal changes (20)(21).…”