EphA2, also known as Ephrin type-A receptor 2, is a receptor tyrosine kinase belonging to the Eph receptor family. Eph receptors and their ephrin ligands form a crucial cell-signaling network. EphA2 is involved in multiple biological processes such as cell proliferation, survival, migration, invasion, angiogenesis, and stem cell-related functions [1-10].

Over 25 years of research has defined EphA2 as a promising molecular target for cancer treatment. It is highly expressed in tumor tissues but at low levels in most normal adult tissues. In breast cancer, its overexpression is linked to poor prognosis, and it plays important roles in malignant breast progression processes like proliferation and metastasis [1]. In hepatocellular carcinoma, the Ephrin-A3/EphA2 axis promotes cancer stemness in a hypoxic microenvironment [2]. In glioblastoma, EphA2 may act as a receptor for PDGFA, and combined inhibition of EphA2 and PDGFRA shows potential as a therapeutic strategy [3]. It also serves as a functional entry receptor for HCMV infection in glioblastoma cells [4].

In conclusion, EphA2 is a key molecule in cancer-related biological processes. Its overexpression in various cancers, as revealed through in-vivo and other functional studies, makes it an attractive therapeutic target. Research on EphA2 using gene-knockout or conditional-knockout mouse models (although not explicitly detailed in the provided abstracts) could potentially further clarify its role in cancer development and progression, offering new insights for cancer treatment strategies. [1-10]