Apatinib Mesylate Inhibits Cell Proliferation and the Metastasis of Esophageal Squamous Cell Carcinoma Through ERK/ELK-1/Snail Pathway.

This study aimed to evaluate the impact of apatinib (APT) mesylate on the growth, migration ability, and underlying mechanisms in esophageal squamous cell carcinoma (ESCC) cell lines Kyse30 and Kyse150. Additionally, the anti-metastatic effects of APT mesylate were further validated in a nude mouse xenograft metastasis model. In vitro, APT mesylate treatment significantly reduced cell viability and migration ability in both cell lines in a dose- and time-dependent manner. Western blot analysis showed that APT mesylate inhibited the expression of proteins involved in the ERK/ELK-1/Snail signaling pathway, including ERK1/2, Snail, N-cadherin, and Vimentin, while upregulating E-cadherin expression. In vivo, APT mesylate administration notably decreased the number of pulmonary metastatic nodules in nude mice, with higher doses showing more pronounced effects. The 200 mg/kg high-dose group exhibited a significantly lower number of metastatic nodules compared to the cisplatin (CIS) group. The results suggest that APT mesylate inhibits ESCC cell proliferation and migration primarily by suppressing the ERK/ELK-1/Snail signaling pathway, which mediates epithelial-mesenchymal transition (EMT) and reduces metastasis and invasiveness. This study provides experimental evidence for the potential clinical application of APT mesylate in targeted therapy for ESCC, indicating its promising clinical value.