Expression of Fas and Fas ligand in human gastric adenomas and intestinal-type carcinomas: correlation with proliferation and apoptosis

Osaki, Mitsuhiko; Kase, Satoru; Kodani, Isamu; Watanabe, M.; Adachi, Hisashi; Ito, Hisao

doi:10.1007/s10120-001-8010-z

Cited by 23 publications

(15 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly to our findings, most authors showed no significant correlations between FasL expression and depth of gastric wall infiltration [7,8,11,13].…”

Section: Discussionsupporting

confidence: 87%

See 1 more Smart Citation

Correlation between Fas and FasL proteins expression in normal gastric mucosa and gastric cancer

Gryko

Guzińska‐Ustymowicz²,

Pryczynicz³

et al. 2011

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

Abstract:The study's objective was to assess the expressions of Fas and FasL proteins in gastric cancer in correlation with chosen clinicohistological parameters. Fas and FasL expression was analyzed in 68 patients with gastric cancer, using the immunohistochemical method. The expression of Fas was found to be lower in gastric cancer cells than in healthy mucosa, both in the lining epithelium and in glandular tubes (28% vs. 48% and 44%; p < 0.001). The expression of FasL was also markedly lower in cancer cells than in glandular tubes, yet higher than in the lining epithelium (51% vs. 73% and 14%; p < 0.01). Positive expressions of FasL and Fas were lower in less advanced gastric cancer cells (T1, T2), than in more advanced tumors (T3, T4), but only in the case of FasL was this difference statistically significant (p < 0.05). Our findings seem to confirm the theory of the impact of apoptotic disorders at the level of Fas receptor and FasL protein in the process of gastric cancer formation and growth, which is manifested in the varied expressions of these proteins in gastric cancer and in the normal lining and glandular epithelium of the stomach. However, the lack of significant differences in the expressions of Fas and FasL in correlation to other clinicohistological parameters indicates the existence of mechanisms that have a greater impact on the process of differentiation of gastric cancers. This in our opinion eliminates these proteins as prognostic factors.

show abstract

“…Similarly to our findings, most authors showed no significant correlations between FasL expression and depth of gastric wall infiltration [7,8,11,13].…”

Section: Discussionsupporting

confidence: 87%

“…This difference, however, was not statistically significant. Also, Osaki et al [11] did not observe any significant differences in Fas expression between adenomas and early and advanced forms of cancer (38% vs. 43% vs. 37%). Similarly, Liu et al [7] found no differences in the expressions of Fas and FasL in relation to cancer advancement.…”

Section: Discussionmentioning

confidence: 88%

Correlation between Fas and FasL proteins expression in normal gastric mucosa and gastric cancer

Gryko

Guzińska‐Ustymowicz²,

Pryczynicz³

et al. 2011

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

show abstract

“…A-to-G substitution at FAS-670 altered FAS transcriptional activity by the disruption of STAT1 binding sequence, the polymorphism of which was earlier pointed out to be associated with the risk of esophageal squamous cell carcinoma (Sun et al 2004) and acute myeloid leukemia (Sibley et al 2003). However, the results of our case-control study did not support this hypothesis, presumably because not all gastric tumors express FAS as reported (positive cases up to 30% of gastric cancer) (Vollmers et al 1997;Osaki et al 2001). Based on previous epidemiological studies of the polymorphism, the positive and negative correlation between the polymorphism and a risk of cervical squamous cell carcinoma has been disregarded (Lai et al 2003;Engelmark et al 2004).…”

Section: Discussioncontrasting

confidence: 56%

A polymorphism of C-to-T substitution at −31 IL1B is associated with the risk of advanced gastric adenocarcinoma in a Japanese population

Ikehara

Matsuo

et al. 2006

J Hum Genet

View full text Add to dashboard Cite

Proinflammatory cytokine gene polymorphisms have been demonstrated to associate with gastric cancer risk, of which IL1B-31T/C and -511C/T changes have been well investigated due to the possibility that they may alter the IL1B transcription. The signal transduction target upon interleukin 1 beta (IL1b) stimulation, the nuclear factor of kappa B (NFjB) activation, supports cancer development, signal transduction in which is mediated by FS-7 cellassociated cell surface antigen (FAS) signaling. Based on recent papers describing the prognostic roles of the polymorphisms and the NFjB functions on cancer development, we sought to determine if Japanese gastric cancer patients were affected by the IL1B -31/ -511 and FAS-670 polymorphisms. A case-control study was conducted on incident gastric adenocarcinoma patients (n=271) and age-gender frequencymatched control subjects (n=271). We observed strong linkage disequilibrium between the T allele at -511 and the C allele at -31 and between the C allele at -511 and the T allele at -31 in IL1B in both the cases and controls (R 2 =0.94). Neither IL1B-31, -511 nor FAS-670 polymorphisms showed significantly different risks of gastric adenocarcinoma. Though FAS-670 polymorphisms did not show any significant difference, the proportion of subjects with IL1B-31TT (or IL1B-511CC) increased according to stage (trend P=0.019). In particular, subjects with stage IV had a two times higher probability of having either IL1B-31TT (or IL1B-511CC) genotype compared with stage I subjects. These observations suggest that IL1B-31TT and IL1B-511CC are associated with disease progression. Abbreviations NFjBNuclear factor of kappa B HP Helicobacter pylori PCR-CTPP Polymerase chain reaction with confronting two-pair primers

show abstract

“…Also recent studies characterising EP receptor expression in a variety of tumour types showed that expression of EP1 is increased in tumour cells relative to normal tissue (Shoji et al, 2004;Miyata et al, 2006;Rask et al, 2006) and is associated with tumour progression and metastasis in prostate cancer (Miyata et al, 2006). Similarly, FasL expression has been shown to be upregulated in tumour cells relative to normal tissue and is associated with tumour progression and metastasis (Mann et al, 1999;Osaki et al, 2001;Belluco et al, 2002). As inhibition of FasL expression in colon cancer cells significantly retards tumour formation in mice (Ryan et al, 2005), these findings suggest that targeting the EP1 receptor may help to prevent or treat colon cancer, in part through preventing FasL upregulation in tumour cells.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 stimulates Fas ligand expression via the EP1 receptor in colon cancer cells

et al. 2008

View full text Add to dashboard Cite

Fas ligand (FasL/CD95L) is a member of the tumour necrosis factor superfamily that triggers apoptosis following crosslinking of the Fas receptor. Despite studies strongly implicating tumour-expressed FasL as a major inhibitor of the anti-tumour immune response, little is known about the mechanisms that regulate FasL expression in tumours. In this study, we show that the cyclooxygenase (COX) signalling pathway, and in particular prostaglandin E 2 (PGE 2 ), plays a role in the upregulation of FasL expression in colon cancer. Suppression of either COX-2 or COX-1 by RNA interference in HCA-7 and HT29 colon tumour cells reduced FasL expression at both the mRNA and protein level. Conversely, stimulation with PGE 2 increased FasL expression and these cells showed increased cytotoxicity against Fas-sensitive Jurkat T cells. Prostaglandin E 2 -induced FasL expression was mediated by signalling via the EP1 receptor. Moreover, immunohistochemical analysis using serial sections of human colon adenocarcinomas revealed a strong positive correlation between COX-2 and FasL (r ¼ 0.722; Po0.0001) expression, and between EP1 receptor and FasL (r ¼ 0.740; Po0.0001) expression, in the tumour cells. Thus, these findings indicate that PGE 2 positively regulates FasL expression in colon tumour cells, adding another pro-neoplastic activity to PGE 2 .

show abstract

Expression of Fas and Fas ligand in human gastric adenomas and intestinal-type carcinomas: correlation with proliferation and apoptosis

Cited by 23 publications

References 37 publications

Correlation between Fas and FasL proteins expression in normal gastric mucosa and gastric cancer

Correlation between Fas and FasL proteins expression in normal gastric mucosa and gastric cancer

A polymorphism of C-to-T substitution at −31 IL1B is associated with the risk of advanced gastric adenocarcinoma in a Japanese population

Prostaglandin E2 stimulates Fas ligand expression via the EP1 receptor in colon cancer cells

Contact Info

Product

Resources

About