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Anlotinib induces tumor blood vessel normalization to strengthen the anticancer effect of radiotherapy on esophageal cancer by inhibiting EphA2


 Background

Anlotinib has anti-tumor activity in diverse solid tumors. Given that, our study was designed to unearth the mechanism of Anlotinib in radioresistant esophageal cancer (EC) cells by modulating Ephrin type-A receptor 2 (EphA2).
Methods

EC cells (TE-1 and KYSE-150) were induced to radioresistant EC cells (TE-1R and KYSE-150R). EphA2 expression in TE-1R and KYSE-150R cells was measured. Then, TE-1R and KYSE-150R cells were treated with Anlotinib and/or transfected with the plasmids that altered EphA2 expression. Otherwise, TE-1R and KYSE-150R cells were transfected with si-EphA2 or OE-EphA2 plasmids independently. In vitro experiments were conducted to monitor cell proliferation, angiogenesis, migration and invasion. In vivo experiment was also implemented to observe tumor growth.
Results

EphA2 expression was raised in TE-1R and KYSE-150R cells. Anlotinib inhibited proliferation, angiogenesis, migration and invasion of TE-1R and KYSE-150R cells in vitro, as well as tumor growth and MVD in vivo. Inhibiting EphA2 enhanced Anlotinib-mediated effects on TE-1R and KYSE-150R cells. Down-regulating EphA2 restrained proliferation, angiogenesis, migration and invasion of TE-1R and KYSE-150R cells.
Conclusion

It is concluded that Anlotinib suppresses EC development under radiotherapy by inhibiting EphA2, providing another perspective to overcome radioresistance in EC.