Expression of TERT in precancerous gastric lesions compared to gastric cancer

Duarte, Márcia Cristina; Babeto, Erica; Leite, Kátia R. M.; Miyazaki, Kenji; Borim, Aldenis Albanese; Rahal, Paula; Silva, A. E.

doi:10.1590/s0100-879x2010007500143

Cited by 12 publications

(14 citation statements)

References 22 publications

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“…In addition, the suppression of hTERT could also inhibit the malignant activity of gastric cancer [26, 27]. Previous studies have shown that the expression of hTERT in human precancerous gastric lesions was higher compared with the normal gastric epithelium, while hTR and hTP1 did not show significant changes [28]. Consistent with a previous study, there is a close association between hTERT and GIM, but the detailed mechanism needs further study.…”

Section: Introductionsupporting

confidence: 73%

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hTERT promotes gastric intestinal metaplasia by upregulating CDX2 via NF-κB signaling pathway

et al. 2017

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BackgroundhTERT has been reported involved in the proliferation and metastasis of gastric cancer, but the role of hTERT in gastric intestinal metaplasia, a premalignant lesion of the gastric mucosa was unknown. The aim of the present study was to investigate the role of hTERT in GIM and the effect of hTERT on CDX2 expression in gastric cells.ResultsExperiments showed that expression of hTERT was significantly higher in GIM than in normal gastric mucosa. Moreover, hTERT increased the KLF4 level via NF-κB during GIM. Furthermore, KLF4 is involved in the up-regulation of CDX2 induced by hTERT, and hTERT can interact with p50, thereby increasing the level of CDX2.Materials and MethodsImmunohistochemistry was used to detect the expression of hTERT in gastric intestinal metaplasia tissue. Then, effect of hTERT on the expression of CDX2 was detected by qRT-PCR, WB and dual luciferase experiment. The role of p65 and p50 in the regulation of CDX2 were further detected by WB, CO-IP and ChIP.ConclusionsWe may conclude that hTERT promotes GIM by up-regulating CDX2 via NF-κB signaling pathway.

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Section: Introductionsupporting

confidence: 73%

“…It has previously been reported that hTERT has a relationship with NF-κB in the nucleus and promotes the expression of NF-κB downstream gene transcription [28]. However, p65 did not bind and influence the promoter activity of CDX2 (Figure 3D).…”

Section: Resultsmentioning

confidence: 76%

hTERT promotes gastric intestinal metaplasia by upregulating CDX2 via NF-κB signaling pathway

et al. 2017

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“…DNA and cDNA samples of gastric biopsies (antrum and corpus) of the lesion area and adjacent normal mucosa stored in our laboratory from a previous study [48] were used. All subjects were recruited from the Service of Endoscopy, Hospital de Base, São José do Rio Preto, SP, Brazil.…”

Section: Methodsmentioning

confidence: 99%

Deregulation of Annexin-A1 and Galectin-1 Expression in Precancerous Gastric Lesions: Intestinal Metaplasia and Gastric Ulcer

Rossi

Duarte

Poltronieri

et al. 2014

Mediators of Inflammation

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Objective. Annexin-A1 (ANXA1/AnxA1) and galectin-1 (LGALS1/Gal-1) are mediators that play an important role in the inflammatory response and are also associated with carcinogenesis. We investigated mRNA and protein expression in precancerous gastric lesions that participate in the progression cascade to gastric cancer, such as intestinal metaplasia (IM) and gastric ulcer (GU). Methods. Quantitative real-time PCR (qPCR) and immunohistochemical techniques were used to analyze the relative quantification levels (RQ) of ANXA1 and LGALS1 mRNA and protein expression, respectively. Results. Increased relative expression levels of ANXA1 were found in 100% of cases, both in IM (mean RQ = 6.22 ± 0.06) and in GU (mean RQ = 6.69 ± 0.10). However, the LGALS1 presented basal expression in both groups (IM: mean RQ = 0.35 ± 0.07; GU: mean RQ = 0.69 ± 0.09). Immunohistochemistry revealed significant positive staining for both the AnxA1 and Gal-1 proteins in the epithelial nucleus and cytoplasm as well as in the stroma of the IM and GU groups (P < 0.05) but absence or low immunorectivity in normal mucosa. Conclusion. Our results bring an important contribution by evidencing that both the AnxA1 and Gal-1 anti-inflammatory proteins are deregulated in precancerous gastric lesions, suggesting their involvement in the early stages of gastric carcinogenesis, possibly due to an inflammatory process in the gastric mucosa.

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“…As new antibodies binding to hTERT have become available and tested for binding specificity, reports of hTERT-expression have emerged. Elevated levels of hTERT in precancerous lesions have been identified in gastric tissue (36), and colonic adenocarcinomas (37). The hTERT protein levels of colonic mucosa may provide insight into the transition from normal-looking mucosal morphology towards a possible colorectal cancer, as normal colonic mucosa has low hTERT levels, whereas colorectal cancers have high levels of hTERT (38).…”

Section: Discussionmentioning

confidence: 99%

Reduced hTERT protein levels are associated with DNA aneuploidy in the colonic mucosa of patients suffering from longstanding ulcerative colitis

Friis-Ottessen

Angelis

Schjølberg

et al. 2014

International Journal of Molecular Medicine

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Longstanding ulcerative colitis (UC) is a disease of chronic inflammation of the colon. It is associated with the development of colorectal cancer through a multistep process including increasing degrees of dysplasia and DNA-ploidy changes. However, not all UC patients will develop these characteristics even during lifelong disease, and patients may therefore be divided into progressors who develop dysplasia or cancer, and non-progressors who do not exhibit such changes. In the present study, the amount of hTERT, the catalytic subunit of the enzyme telomerase, was estimated by using peroxidase immunohistochemistry (IHC) in a set of progressor and non-progressor UC colectomies. The protein levels in the colonic mucosa of the progressors and non-progressors were compared, and further comparisons between different categories of dysplastic development and to DNA-ploidy status within the progressors were made. Levels of hTERT were elevated in the colonic mucosa of the progressors and non-progressors when compared to non-UC control samples, but no difference was observed between the hTERT levels in the mucosa of progressors and non-progressors. The levels of hTERT associated with levels of Ki67 to a significant degree within the non-progressors. hTERT expression in lesions with DNA-aneuploidy were decreased as compared to diploid lesions, when stratified for different classes of colonic morphology. Our results indicate an association between hTERT protein expression and aneuploidy in UC-progressor colons, and also a possible protective mechanism in the association between hTERT and Ki67, against development of malignant features within the mucosa of a UC-colon.

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Expression of TERT in precancerous gastric lesions compared to gastric cancer

Cited by 12 publications

References 22 publications

hTERT promotes gastric intestinal metaplasia by upregulating CDX2 via NF-κB signaling pathway

hTERT promotes gastric intestinal metaplasia by upregulating CDX2 via NF-κB signaling pathway

Deregulation of Annexin-A1 and Galectin-1 Expression in Precancerous Gastric Lesions: Intestinal Metaplasia and Gastric Ulcer

Reduced hTERT protein levels are associated with DNA aneuploidy in the colonic mucosa of patients suffering from longstanding ulcerative colitis

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