Regulation of cagA-Helicobacter on gastric PIM2 expression in gastric cancer.

IF 2.2 4区医学 Q3 ONCOLOGY

Cancer Biomarkers Pub Date : 2024-01-01 DOI:10.3233/CBM-230351

Wenjuan Liang, Haiyan Wang, Lijuan Hong, Wenting Cao, Shuaiyin Chen, Rongguang Zhang

{"title":"Regulation of cagA-Helicobacter on gastric PIM2 expression in gastric cancer.","authors":"Wenjuan Liang, Haiyan Wang, Lijuan Hong, Wenting Cao, Shuaiyin Chen, Rongguang Zhang","doi":"10.3233/CBM-230351","DOIUrl":null,"url":null,"abstract":"Background: The association between infection with cagA-positive H. pylori and an elevated susceptibility to gastric cancer has been firmly established. PIM2 is known to be overexpressed in various types of cancers; however, the specific mechanism by which cagA influences the regulation of PIM2 expression in gastric cancer remains unidentified at present.Materials and methods: A mutant NCTC11637ΔcagA strain of H. pylori and the eukaryotic expression vector pcDNA-cagA were constructed for evaluating PIM2 expression levels in gastric cancer cells (HGC27, SGC7901, and AG) co-cultured with the NCTC11637 and NCTC11637ΔcagA strain, as well as pcDNA-cagA and the empty vector pcDNA3.1 (+).Results: Co-culturing gastric cancer cells with NCTC11637 significantly increased PIM2 expression levels (P< 0.001) compared to the negative control group. Additionally, the expression of PIM2 in cells co-cultured with NCTC11637 was higher than that co-cultured with NCTC11637ΔcagA (P< 0.001). Furthermore, successful construction of the eukaryotic expression vector pcDNA-cagA resulted in a significant increase in PIM2 mRNA expression levels after its transfection into gastric cancer cells compared to the control group after 48 hours.Conclusions: The findings indicate that H. pylori/cagA A could be one of the key factors in regulating PIM2 expression levels, potentially influencing the progression of H. pylori-related Gastric Cancer.","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":" ","pages":"93-101"},"PeriodicalIF":2.2000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11491992/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Biomarkers","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3233/CBM-230351","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: The association between infection with cagA-positive H. pylori and an elevated susceptibility to gastric cancer has been firmly established. PIM2 is known to be overexpressed in various types of cancers; however, the specific mechanism by which cagA influences the regulation of PIM2 expression in gastric cancer remains unidentified at present.

Materials and methods: A mutant NCTC11637ΔcagA strain of H. pylori and the eukaryotic expression vector pcDNA-cagA were constructed for evaluating PIM2 expression levels in gastric cancer cells (HGC27, SGC7901, and AG) co-cultured with the NCTC11637 and NCTC11637ΔcagA strain, as well as pcDNA-cagA and the empty vector pcDNA3.1 (+).

Results: Co-culturing gastric cancer cells with NCTC11637 significantly increased PIM2 expression levels (P< 0.001) compared to the negative control group. Additionally, the expression of PIM2 in cells co-cultured with NCTC11637 was higher than that co-cultured with NCTC11637ΔcagA (P< 0.001). Furthermore, successful construction of the eukaryotic expression vector pcDNA-cagA resulted in a significant increase in PIM2 mRNA expression levels after its transfection into gastric cancer cells compared to the control group after 48 hours.

Conclusions: The findings indicate that H. pylori/cagA A could be one of the key factors in regulating PIM2 expression levels, potentially influencing the progression of H. pylori-related Gastric Cancer.

查看原文本刊更多论文

cagA-Helicobacter 对胃癌中胃 PIM2 表达的调控。

背景：感染 cagA 阳性幽门螺杆菌与胃癌易感性升高之间的关系已被证实。已知 PIM2 在各种癌症中过度表达；然而，目前 cagA 影响胃癌中 PIM2 表达调控的具体机制仍未确定：构建幽门螺杆菌突变株NCTC11637ΔcagA和真核表达载体pcDNA-cagA，用于评估与NCTC11637和NCTC11637ΔcagA株以及pcDNA-cagA和空载体pcDNA3.1（+）共培养的胃癌细胞（HGC27、SGC7901和AG）中PIM2的表达水平：结果：与阴性对照组相比，与 NCTC11637 共培养胃癌细胞可显著提高 PIM2 的表达水平（P< 0.001）。此外，与 NCTC11637 共培养的细胞中 PIM2 的表达高于与 NCTC11637ΔcagA 共培养的细胞（P< 0.001）。此外，成功构建真核表达载体 pcDNA-cagA 后，与对照组相比，转染胃癌细胞 48 小时后 PIM2 mRNA 表达水平显著增加：结论：研究结果表明，幽门螺杆菌/cagA A可能是调节PIM2表达水平的关键因素之一，有可能影响幽门螺杆菌相关胃癌的进展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cancer Biomarkers ONCOLOGY-

CiteScore

5.20

自引率

3.20%

发文量

195

审稿时长

3 months

期刊介绍： Concentrating on molecular biomarkers in cancer research, Cancer Biomarkers publishes original research findings (and reviews solicited by the editor) on the subject of the identification of markers associated with the disease processes whether or not they are an integral part of the pathological lesion. The disease markers may include, but are not limited to, genomic, epigenomic, proteomics, cellular and morphologic, and genetic factors predisposing to the disease or indicating the occurrence of the disease. Manuscripts on these factors or biomarkers, either in altered forms, abnormal concentrations or with abnormal tissue distribution leading to disease causation will be accepted.