Pharmaceutical inhibition of AXL suppresses tumor growth and invasion of esophageal squamous cell carcinoma | Zendy

Sha Han | Zendy; Yequan Wang | Zendy; Chengyan Ge | Zendy; Mingtao Gao | Zendy; Xintong Wang | Zendy; Feiyu Wang | Zendy; Lei Sun | Zendy; Sheng Li | Zendy; Tingting Dong | Zendy; Zhen Dang | Zendy; Wen Cui | Zendy; Guoan Zhang | Zendy; Ning Liu | Zendy

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Pharmaceutical inhibition of AXL suppresses tumor growth and invasion of esophageal squamous cell carcinoma

Author(s) -

Sha Han,

Yequan Wang,

Chengyan Ge,

Mingtao Gao,

Xintong Wang,

Feiyu Wang,

Lei Sun,

Sheng Li,

Tingting Dong,

Zhen Dang,

Wen Cui,

Guoan Zhang,

Ning Liu

Publication year - 2020

Publication title -

experimental and therapeutic medicine

Language(s) - English

Resource type - Journals

eISSN - 1792-1015

pISSN - 1792-0981

DOI - 10.3892/etm.2020.9169

Subject(s) - protein kinase b , cancer research , cell cycle , mmp2 , oncogene , cell growth , mapk/erk pathway , mmp9 , receptor tyrosine kinase , cell , cancer , biology , metastasis , signal transduction , medicine , downregulation and upregulation , microbiology and biotechnology , biochemistry , genetics , gene

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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