Pepsinogen I and II expressions in situ and their correlations with serum pesignogen levels in gastric cancer and its precancerous disease

Li, Ping; He, Caiyun; Sun, Liping; Dong, Ning; Yuan, Yuan

doi:10.1186/1472-6890-13-22

Cited by 17 publications

(18 citation statements)

References 17 publications

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“…Besides the host genetics, histological PGC expression could also be affected by several other factors such as status of gastric mucosa, location of affected or selected tissues, and state of H. pylori infection. Especially, the status of gastric mucosa and the location of tissue have significant effects on in situ PGC expression levels as described in previous studies [16] , [17] . Therefore, detection of histological PGC protein in cancerous tissues could not be accomplished in experimental practice.…”

Section: Discussionmentioning

confidence: 60%

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PGC TagSNP and Its Interaction with H. pylori and Relation with Gene Expression in Susceptibility to Gastric Carcinogenesis

Sun

et al. 2014

PLoS ONE

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BackgroundPepsinogen C (PGC) plays an important role in sustaining the cellular differentiation during the process of gastric carcinogenesis. This study aimed to assess the role of PGC tagSNPs and their interactions with Helicobacter pylori (H. pylori) in the development of gastric cancer and its precursor, atrophic gastritis.MethodsFour PGC tagSNPs (rs6941539, rs6912200, rs3789210 and rs6939861) were genotyped by Sequenom MassARRAY platform in a total of 2311 subjects consisting of 642 gastric cancer, 774 atrophic gastritis, and 895 healthy control subjects. The mRNA and protein expression levels of PGC in gastric tissues and in serum were respectively measured by quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR), immunohistochemistry, and Eenzyme-linked immunoabsorbent assay (ELISA).ResultsWe found associations between PGC rs3789210 CG/GG genotypes and reduced gastric cancer risk and between PGC rs6939861 A variant allele and increased risks of both gastric cancer and atrophic gastritis. As for the haplotypes of PGC rs6941539-rs6912200-rs3789210-rs6939861 loci, the TTCA and TTGG haplotypes were respectively associated with increased and reduced risks of both gastric cancer and atrophic gastritis; additionally, the CTCA haplotype was associated with increased atrophic gastritis risk. Very interestingly, rs6912200 CT/TT genotypes had a positive interaction with H. pylori, synergistically elevating the gastric cancer risk. Moreover, healthy subjects who carried rs6912200 CT, TT and CT/TT variant genotypes had lower histological and serum expression levels of PGC protein.ConclusionsOur findings highlight an important role of PGC rs3789210 and rs6939861 in altering susceptibility to atrophic gastritis and/or gastric cancer. Moreover, people who carry rs6912200 variant genotypes exhibit higher gastric cancer risk in case of getting H. pylori infection, which strongly suggest a necessity of preventing and/or eliminating H. pylori infection in those individuals.

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Section: Discussionmentioning

confidence: 60%

“…Streptavidin-peroxidase two-step immunostaining was then performed according to kit instructions (Kit-9801D2, Maixin Company, Fujian, China). A more detailed method for detecting PGC protein in situ has been described previously [17] .…”

Section: Methodsmentioning

confidence: 99%

PGC TagSNP and Its Interaction with H. pylori and Relation with Gene Expression in Susceptibility to Gastric Carcinogenesis

Sun

et al. 2014

PLoS ONE

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“…Increased circulating pepsinogen levels and increased leakage of plasma protein into the gastric lumen are typical of parasitised animals [ 49 , 50 ] and are probably caused more by inflammation than by worm chemicals. Hyperpepsinogenaemia is considered to be evidence of a leaky abomasal mucosa in many forms of gastritis and is used as a marker for human Helicobacter pylori infection [ 47 , 48 ]. Eosinophils accumulated at the base of the gastric glands ( Fig 4 ) where the chief cells are located, supporting a role for greater permeability in the gland region where pepsinogen is secreted.…”

Section: Discussionmentioning

confidence: 99%

“…Increased mucosal permeability is a major contributor to hyperpepsinogenaemia associated with parasitism, as well as other forms of gastritis [ 47 , 48 ], and leakage of plasma protein and pepsinogen into the gastric lumen [ 49 , 50 ]. The relative importance of direct effects of ES products, physical contact with parasites and inflammation have not been established.…”

Section: Introductionmentioning

confidence: 99%

Abomasal dysfunction and cellular and mucin changes during infection of sheep with larval or adult Teladorsagia circumcincta

et al. 2017

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This is the first integrated study of the effects on gastric secretion, inflammation and fundic mucins after infection with L3 T. circumcincta and in the very early period following transplantation of adult worms. At 3 months-of-age, 20 Coopworth lambs were infected intraruminally with 35,000 L3; infected animals were killed on Days 5, 10, 15, 20 and 30 post-infection and 6 controls on either Day 0 or 30 post-infection. Another 15 Romney cross lambs received 10,000 adult worms at 4–5 months-of-age though surgically-implanted abomasal cannulae and were killed after 6, 12, 24 and 72 hours; uninfected controls were also killed at 72 hours. Blood was collected at regular intervals from all animals for measurement of serum gastrin and pepsinogen and abomasal fluid for pH measurement from cannulated sheep. Tissues collected at necropsy were fixed in Bouin’s fluid for light microscopy, immunocytochemistry and mucin staining and in Karnovsky's fluid for electron microscopy. Nodules around glands containing developing larvae were seen on Day 5 p.i., but generalised effects on secretion occurred only after parasite emergence and within hours after transplantation of adult worms. After L3 infection, there were maximum worm burdens on Days 10–15 post-infection, together with peak tissue eosinophilia, inhibition of gastric acid secretion, hypergastrinaemia, hyperpepsinogenaemia, loss of parietal cells, enlarged gastric pits containing less mucin and increased numbers of mucous neck cells. After adult transplantation, serum pepsinogen was significantly increased after 9 hours and serum gastrin after 18 hours. Parallel changes in host tissues and the numbers of parasites in the abomasal lumen suggest that luminal parasites, but not those in the tissues, are key drivers of the pathophysiology and inflammatory response in animals exposed to parasites for the first time. These results are consistent with initiation of the host response by parasite chemicals diffusing across the surface epithelium, possibly aided by components of ES products which increased permeability. Parietal cells appear to be a key target, resulting in secondary increases in serum gastrin, pit elongation, loss of surface mucins and inhibition of chief cell maturation. Inflammation occurs in parallel, and could either cause the pathology or exacerbate the direct effects of ES products.

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“…Zoalfaghari A et al have proved that the PGI and PGI/II ratio are significantly decreased in AG patients compared with the controls, and these two factors are potential biomarkers for screening AG with high sensitivity and specificity [14]. Ping L et al have indicated that the serum PGI, PGII, and PGI/II ratio are closely related to the occurrence of GC and its precancerous disease [15]. Zhang XM et al have confirmed that patients with early and advanced GC have a significantly lower PGI/II ratio than patients with AG [16].…”

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confidence: 99%

Serum miR-101-3p combined with pepsinogen contributes to the early diagnosis of gastric cancer

et al. 2020

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Background: This study aimed to explore the diagnostic value of serum miR-101-3p combined with pepsinogen (PG) on early diagnosis of gastric cancer (GC). Methods: A total of 61 atrophic gastritis (AG) and 86 GC patients, and 50 healthy volunteers were enrolled. The serum expression of miR-101-3p was measured by qRT-PCR. The serum content of carcinoembryonic antigen (CEA) was measured by Electrochemiluminescence immunoassay. The serum contents of PGI and PGII were measured by Enzyme linked immunosorbent assay. The diagnostic value of serum markers on AG and GC was analyzed by receiver operating characteristic (ROC) analysis.Results: The expression of miR-101-3p, the content of PGI and the ratio of PGI/II were significantly decreased, and the content of PGII was significantly increased in AG patients compared with those in normal controls. The changes of the above serum indicators were more obvious in GC patients than those in AG patients. The content of CEA was significantly higher in GC patients than that in AG patients. In addition, the expression of miR-101-3p was negatively associated with the submucosal infiltration in GC patients. MiR-101-3p exhibited high diagnostic value on AG (AUC 0.8493, sensitivity 80.33%, specificity 80%) and GC (AUC 0.8749, sensitivity 72.09%, specificity 86.49%). MiR-101-3p + PGI + PGI/II (AUC 0.856, sensitivity 80.23%, specificity 77.05%) exhibited a high diagnostic value in distinguishing between AG and GC.Conclusions: MiR-101-3p was a potential diagnostic marker for AG and GC. MiR-101-3p + PGI + PGI/II was effective in distinguishing between AG and GC.

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Pepsinogen I and II expressions in situ and their correlations with serum pesignogen levels in gastric cancer and its precancerous disease

Cited by 17 publications

References 17 publications

PGC TagSNP and Its Interaction with H. pylori and Relation with Gene Expression in Susceptibility to Gastric Carcinogenesis

PGC TagSNP and Its Interaction with H. pylori and Relation with Gene Expression in Susceptibility to Gastric Carcinogenesis

Abomasal dysfunction and cellular and mucin changes during infection of sheep with larval or adult Teladorsagia circumcincta

Serum miR-101-3p combined with pepsinogen contributes to the early diagnosis of gastric cancer

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