ArticleInternational journal of ophthalmology2021
YM155 inhibits retinal pigment epithelium cell survival through EGFR/MAPK signaling pathway.
Article in International journal of ophthalmology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- JNK inhibitor SP600125 alleviates TGF-β2-induced epithelial-mesenchymal transition in RPE cellInternational journal of ophthalmology · 2026Article
- The epidermal growth factor receptor regulates YAP signalling and promotes diabetic retinal fibrosis by modulating the degradation of SAV1.Journal of translational medicine · 2025Article
- Inhibition of EGFR attenuates EGF-induced activation of retinal pigment epithelium cellInternational journal of ophthalmology · 2024Article
- Survivin inhibition attenuates EGF-induced epithelial mesenchymal transformation of human RPE cells via the EGFR/MAPK pathway.PloS one · 2024Article
- Co-Expression of Podoplanin and CD44 in Proliferative Vitreoretinopathy Epiretinal Membranes.International journal of molecular sciences · 2023Review
- Hydrogen peroxide-induced oxidative damage and protective role of peroxiredoxin 6 protein via EGFR/ERK signaling pathway in RPE cells.Frontiers in aging neuroscience · 2023Article
- Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate YM155's effect on retinal pigment epithelium (RPE) cells' viability and the potential regulatory mechanisms.
methodsHuman immortalized RPE cell lines (ARPE-19 cell line) were processed with YM155 and epidermal growth factor (EGF). ARPE-19 cell viability was detected by methyl thiazolyl tetrazolium assay, and apoptosis was tested by flow cytometry assay. ARPE-19 cell proliferation was assessed with bromodeoxyuridine tagged incorporation assay, and migration ability was evaluated
resultsYM155 suppressed ARPE-19 cells' viability in a time and concentration-dependent manner. A high dose of YM155 caused a small amount of ARPE-19 cell death. YM155 significantly diminished the ARPE-19 cells' proliferative and migrative capacity. YM155 down-regulated total EGFR and phosphorylated external signal-regulated protein kinase (ERK), and it up-regulated the phosphorylation of P38MAPK and c-Jun N-terminal kinase (JNK). YM155 induced endocytosis of EGFR in ARPE-19 cell. YM155 also attenuated EGF-induced ARPE-19 cells' proliferative and migrative capacity. Moreover, YM155 significantly decreased the expression of phosphorylated EGFR and ERK after treated by EGF.
conclusionYM155 inhibits RPE cell survival, the cell proliferative and migrative capacity, and it effectuates a small amount of cell death through the EGFR/MAPK signaling pathway. YM155 might, therefore, be an agent to prevent and treat abnormal RPE cell survival in proliferative vitreoretinopathy.
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