ArticleExperimental and therapeutic medicine2019
Cadmium induces A549 cell migration and invasion by activating ERK.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- ATP purinergic receptor signalling promotes Sca-1Cell communication and signaling : CCS · 2023Article
- CCL2 promotes proliferation, migration and angiogenesis through the MAPK/ERK1/2/MMP9, PI3K/AKT, Wnt/β‑catenin signaling pathways in HUVECs.Experimental and therapeutic medicine · 2023Article
- FLLL32 Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells by Regulating the p38 Pathway.International journal of molecular sciences · 2021Article
- A narrative review of the migration and invasion features of non-small cell lung cancer cells upon xenobiotic exposure: insights fromTranslational lung cancer research · 2021Review
- TGF-β Induced CTGF Expression in Human Lung Epithelial Cells through ERK, ADAM17, RSK1, and C/EBPβ Pathways.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cadmium (Cd) is an established carcinogen that is involved in the progression of lung cancer. However, the mechanisms underlying this Cd-induced process have yet to be fully elucidated. The present study explored the potential roles of phosphorylated (p)-ERK in the Cd-induced migration and invasion of lung cancer cells. An MTT assay was performed to evaluate cell viability whilst western blot analysis and reverse transcription-quantitative PCR were used to detect the expression of protein and mRNA, respectively. Migration and invasion assays were performed to assess cell migratory and invasive abilities. The results demonstrated that exposure to Cd increased the expression of p-ERK in A549 cells. Cd also enhanced the migration and invasion of A549 cells, which could be blocked via U0126 treatment (an inhibitor of mitogen activated protein kinase). In addition, it was identified that Cd-induced expression of matrix metalloproteinases 2 mRNA was mediated by p-ERK. In conclusion, the present findings indicated that Cd induced A549 cell migration and invasion by activating ERK, and it was hypothesized that p-ERK could serve as a target in the clinical treatment of Cd-induced lung cancer.
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