Effect of Helicobacter pylori on apoptosis and apoptosis related genes in gastric cancer cells

Yang, Yi; Deng, Chaolin; Peng, Jun; Wong, Benjamin C Y; Lam, Sum; Xia, Harry H.X.

doi:10.1136/mp.56.1.19

Cited by 40 publications

(39 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, Bax was detected in all groups with the highest expression in the group with H pylori infection alone, which also presented Bcl-2 expression as mentioned above. Although some authors have shown an increased Bcl-2 expression in H pylori-positive cases, in the group (Hp+/EBV-) the Bcl-2 expression was very low [33][34][35][36][37] . Although it was not statistically significant, our findings suggest a possible correlation between H pylori and Bcl-2 expression, unlike with EBV.…”

Section: Discussionmentioning

confidence: 99%

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

Lima

Lima²,

André³

et al. 2008

WJG

View full text Add to dashboard Cite

AIM: To investigate the interrelationship betweenH pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression.METHODS: seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc, Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation. RESULTS:The positivity rates for H pylori and EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive cases were also H pylori positive. None infectious agent was observed in 5.55% of the cases. The intestinal type tumor was more frequent in the co-infected and non-infected groups. The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P = 0.039). The Bcl-2 was only detected in the group exclusively infected by H pylori .However, c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group. Mutation of p53 was present in all groups, with the highest frequencies in the H pylori positive groups. CONCLUSION:The frequency of H pylori infection in gastric carcinomas was high. The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents, suggesting a possible involvement of H pylori with apoptotic process. The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins. Nevertheless, p53 mutation shows to be a relevant alteration, independent of both infectious agents.

show abstract

Section: Discussionmentioning

confidence: 99%

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

Lima

Lima²,

André³

et al. 2008

WJG

View full text Add to dashboard Cite

show abstract

“…Yang et al [66] described that H pylori induces apoptosis in human gastric adenocarcinoma cells mediated by an increased expression of MYC mRNA.…”

Section: Myc and Gastric Carcinogenesismentioning

confidence: 99%

MYC and gastric adenocarcinoma carcinogenesis

Calcagno¹,

Leal²,

Assumpção³

et al. 2008

WJG

View full text Add to dashboard Cite

MYC is an oncogene involved in cell cycle regulation, cell growth arrest, cell adhesion, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer.In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma c a r c i n o g e n e s i s , i n c l u d i n g i t s a s s o c i a t i o n w i t h Helicobacter pylori (H pylori ) MYC AND CANCERMYC gene was found to be the cellular homolog of retroviral v-myc oncogene about 30 years ago [12][13][14] . It is located on chromosomal region 8q24.1, has 3 exons [15,16] and encodes a nuclear phosphoprotein [17] . MYC has to heteromerize with MAX, a protein expressed constitutively, to acquire DNA-binding activity. MYC/MAX dimmers are made viable by a basic region helix-loop-helix leucine-zipper motif (bHLHZip), conserved sequences in the carboxyl terminus of both proteins. MYC/MAX dimmers bind to E-box sequence CACGTG in the promoters of specific target genes and stimulate their transcription [18] . MYC has an effect on up to about 15% of genes in genomes of many organisms, from flies to humans [19] . Groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the Myc target gene network.MYC also consistently represses genes involved in cell growth arrest and cell adhesion [20] . Dominguez-Sola et al [21] recently showed that Myc interacts with the prereplicative complex and localizes to early sites of DNA synthesis. Thus, it also has a direct role in the control of DNA replication.MYC regulates transcription from its targets through several mechanisms, including recruitment of histone acetylases, chromatin modulating proteins, basal transcription factors and DNA methyltransferase [22][23][24][25][26] . Protein products of MYC target genes g o on to mediate the downstream effects of MYC on cell biology. MYC is then rapidly degraded, and the pathway switches to a transcriptionally repressive state when MAX dimerizes with a group of related bHLH-Zip proteins, the MAD family, that act as MYC antagonists [27] ( Figure 1).MYC expression might be regulated transcriptionally (initiation and elongation), post-transcriptionally (mRNA stability and translation) or post-translationally (protein stability) [28] . MYC is generally recognized as an important regulator of proliferation, growth, differentiation and apoptosis [29,30] . Therefore, it is also accepted that the deregulation of MYC expression is a major event in cancer pathogenesis or progression. Deregulated expression of a wild-type MYC protein is suff...

show abstract

“…Fas-mediated apoptosis in gastric cells was also described upon infection by H. pylori, however in this case other apoptotic factors are involved as well. These include TRIAL and its receptor subtypes (Yang, et al 2003;Martin et al, 2004). Because the binding of Fas ligand (FasL) to the Fas antigen results in the transduction of a cytolytic signal into the cell followed by apoptosis, cells overexpressing GKN1 showed an increase in apoptosis that is mainly due to the exposure of the MKN28 cells to FasL with respect to that observed in the absence of FasL.…”

Section: Evaluation Of Transient Expression Of Gkn1 In Gastric Cancermentioning

confidence: 98%

Role of Gastrokine 1 in Gastric Cancer

Rippa¹,

Mallardo²,

Arcari³

2011

Gastritis and Gastric Cancer - New Insights in Gastroprotection, Diagnosis and Treatments

View full text Add to dashboard Cite

Effect of Helicobacter pylori on apoptosis and apoptosis related genes in gastric cancer cells

Cited by 40 publications

References 30 publications

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

MYC and gastric adenocarcinoma carcinogenesis

Role of Gastrokine 1 in Gastric Cancer

Contact Info

Product

Resources

About