ArticleMolecular medicine reports2016
N-methyl-N-nitro-N'-nitrosoguanidine induces the expression of CCR2 in human gastric epithelial cells promoting CCL2-mediated migration.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Renqing Mangjue modulates chronic atrophic gastritis inflammation-cancer transition via the cGMP-PKG/PI3K-AKT pathway.Chinese medicine · 2026Article
- From inflammation to carcinogenesis: MiRNA regulates epithelial-mesenchymal transition to facilitate malignant progression of gastric precancerous lesions.Frontiers in oncology · 2026Review
- A novel cycloastragenol-encapsulated carboxymethyl chitosan-silk fibroin hydrogel combined with sucralfate alleviates MNNG-induced chronic atrophic gastritis by targeting HIF-1α and VEGF signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Ursolic and oleanolic acids suppress MNNG induced malignant transformation of human gastric mucosal epithelium by regulating the PI3 K/AKT pathway.Scientific reports · 2025Article
- Investigation of c-Fos/c-Jun Signaling Pathways in Periostracum Cicadae's Inhibition of EMT in Gastric Tissue.Pharmaceuticals (Basel, Switzerland) · 2025Article
- OLFM4 promotes the progression of intestinal metaplasia through activation of the MYH9/GSK3β/β-catenin pathway.Molecular cancer · 2024Article
- Crocin reverses 1-methyl-3-nitroso-1-nitroguanidine (MNNG)-induced malignant transformation in GES-1 cells through the Nrf2/Hippo signaling pathway.Journal of gastrointestinal oncology · 2020Article
- miR-374 mediates the malignant transformation of gastric cancer-associated mesenchymal stem cells in an experimental rat model.Oncology reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation has a decisive role in tumorigenesis, particularly in gastric carcinogenesis. The CC chemokine ligand 2 (CCL2), an important inflammatory cytokine, is involved in the initiation, development and progression of various types of cancer. However, the role of CCL2 in gastric cancer remains to be elucidated. The present study demonstrated that recombinant CCL2 stimulation caused no effect on the morphology, proliferation and migration of human GES-1 gastric mucosa epithelial cells, in which the protein expression of CC-chemokine receptor 2 (CCR2) was markedly low. However, the expression of CCR2 was significantly upregulated in the GES-1 cells following pretreatment with the chemical carcinogen, N-methyl-N-nitro-N'-nitrosoguanidine (MNNG), for 12 h or transformed with MNNG (MC cells). The present study used CCL2 to stimulate MNNG pretreated GES-1 cells and MC cells, and demonstrated that CCL2 clearly promoted their migration and the epithelial-mesenchymal transition (EMT). However, no effect was observed on the proliferative ability of the cells. Taken together, these findings suggested that the CCL2/CCR2 chemokine signaling may regulate the EMT in gastric epithelial cells and resulted in gastric carcinogenesis in response to the intake of the carcinogen, MNNG.
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