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调控 cagA-幽门螺杆菌对胃癌中 PIM2 表达的影响。

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

机构信息

School of Public Health, Hainan Medical University, Haikou, China.

Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, China.

出版信息

Cancer Biomark. 2024;41(2):93-101. doi: 10.3233/CBM-230351.

DOI:10.3233/CBM-230351
PMID:39331090
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11491992/
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.

摘要

背景

cagA 阳性幽门螺杆菌感染与胃癌易感性增加之间的关联已得到证实。PIM2 已知在多种类型的癌症中过表达；然而，目前尚不清楚 cagA 如何影响胃癌中 PIM2 表达的调节。

材料和方法

构建了幽门螺杆菌突变株 NCTC11637ΔcagA 和真核表达载体 pcDNA-cagA，用于评估共培养 NCTC11637 和 NCTC11637ΔcagA 菌株以及 pcDNA-cagA 和空载体 pcDNA3.1(+)的胃癌细胞（HGC27、SGC7901 和 AG）中 PIM2 表达水平。

结果

与阴性对照组相比，共培养胃癌细胞与 NCTC11637 可显著增加 PIM2 表达水平（P<0.001）。此外，与 NCTC11637ΔcagA 共培养的细胞中 PIM2 的表达高于与 NCTC11637 共培养的细胞（P<0.001）。此外，成功构建了真核表达载体 pcDNA-cagA，转染胃癌细胞 48 小时后，与对照组相比，PIM2mRNA 表达水平显著增加。

结论

这些发现表明，H. pylori/cagA A 可能是调节 PIM2 表达水平的关键因素之一，可能影响与 H. pylori 相关的胃癌的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/15e495be02ca/cbm-41-cbm230351-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/306a62454f99/cbm-41-cbm230351-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/4c05661d089f/cbm-41-cbm230351-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/0a556b8df9c8/cbm-41-cbm230351-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/aad69aabc48d/cbm-41-cbm230351-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/15e495be02ca/cbm-41-cbm230351-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/306a62454f99/cbm-41-cbm230351-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/4c05661d089f/cbm-41-cbm230351-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/0a556b8df9c8/cbm-41-cbm230351-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/aad69aabc48d/cbm-41-cbm230351-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0460/11491992/15e495be02ca/cbm-41-cbm230351-g005.jpg

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本文引用的文献

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PIM2 Expression Induced by Proinflammatory Macrophages Suppresses Immunotherapy Efficacy in Hepatocellular Carcinoma.
促炎巨噬细胞诱导的 PIM2 表达抑制肝癌的免疫治疗疗效。
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