| Downregulation of EphA2 significantly inhibited invasion, proliferation and clonogenicity in vitro and suppressed tumorigenicity in vivo. Data provides the first in vivo evidence demonstrating a direct role for EphA2 in promoting melanoma tumorigenicity. | skin, |
| EphA2 acts as a KRas cooperative tumor suppressor | None |
| EphA2 increases as prostatic epithelial cells have more aggressive phenotype. EphA2 functions as a powerful oncogene. Presence of high levels of EphA2 suggests opportunities for prostate cancer prevention and treatment. | prostate, |
| EphA2 is a critical oncogene in melanoma. | skin, |
| EphA2 is a critical oncogene in melanoma. | skin, |
| results identify EphA2, a tyrosine kinase with known functions in neovascularization and oncogenesis, as an entry receptor for Kaposi_s sarcoma-associated herpesvirus | sarcoma, |
| miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene. | breast, |
| The activation of the EphA2 receptor tyrosine kinase can inhibit a major oncogenic signaling pathway, the Akt-mTORC1 pathway. | None |
| These findings implicate EphB6 as a negative regulator of EphA2 oncogenic signaling. | None |
| Claudin-4 controls the receptor tyrosine kinase EphA2 pro-oncogenic switch through beta-catenin | None |