Evidence map›Paper›PMID 39331090›Full record

ArticleCancer biomarkers : section A of Disease markers2024

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

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

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Article in Cancer biomarkers : section A of Disease markers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Wenjuan LiangSchool of Public Health, Hainan Medical University, Haikou, China.
Haiyan WangDepartment of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, China.
Lijuan HongHospital-Acquired Infection Control Department, First Affiliated Hospital, Hainan Medical University, Haikou, China.
Wenting CaoSchool of Public Health, Hainan Medical University, Haikou, China.
Shuaiyin ChenDepartment of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, China.
Rongguang ZhangDepartment of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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

methodsA 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 (+).

resultsCo-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.

conclusionsThe 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.

Indexed as

Antigens, BacterialBacterial ProteinsHelicobacter pyloriProtein Serine-Threonine KinasesProto-Oncogene ProteinsStomach NeoplasmsCell Line, TumorCoculture TechniquesGene Expression Regulation, NeoplasticHelicobacter InfectionsHumansAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriPIM2 protein, humanProtein Serine-Threonine KinasesProto-Oncogene ProteinsCagAGastric cancerHelicobacter pyloriPIM2regulation

Identifiers

PMID39331090
PMCPMC11491992

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