ArticleExperimental and therapeutic medicine2020
Pharmaceutical inhibition of AXL suppresses tumor growth and invasion of esophageal squamous cell carcinoma.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- AXL is associated with STAT3 activation in breast cancer.Molecular and clinical oncology · 2026Article
- A Bioinformatic Assay of Quercetin in Gastric Cancer.International journal of molecular sciences · 2024Article
- AXL upregulates c‑Myc expression through AKT and ERK signaling pathways in breast cancers.Molecular and clinical oncology · 2023Article
- KISS-1, Mediated by Promoter Methylation, Suppresses Esophageal Squamous Cell Carcinoma Metastasis via MMP2/9/MAPK Axis.Digestive diseases and sciences · 2022Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is a common type of cancer in a number of regions of the world, including East Asia, South Africa and Iran. It is often associated with poor prognosis rates. Tyrosine-protein kinase receptor UFO (AXL) is overexpressed in a subset of ESCC tumors, therefore the present study aimed to determine the effect of R428, a selective inhibitor of AXL, on ESCC tumor cells. TE1 and KYSE150 cell lines were used as models to investigate the effects of R428 treatment. The proliferative rate of the tumor cells was analyzed using MTT and colony formation assays. In addition, cell migration and invasion rates were analyzed using wound healing and Matrigel assays, respectively. The expression levels of matrix metalloproteinase (MMP)2 and MMP9, and the activation of protein kinase B (AKT), extracellular signal-regulated kinase (ERK) and AXL signaling were analyzed using gelatin zymography and western blotting. The results revealed that R428 inhibited the proliferative and invasive abilities of both cell lines. Furthermore, AXL, AKT and ERK signaling were all decreased in response to R428 treatment, alongside the expression levels of MMP2 and MMP9. In conclusion, the results of the present study suggested that R428 treatment may suppress ESCC tumor cell proliferation and invasion, representing a potential therapeutic target for ESCC.
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