Cell Death Dis: EphA2 Y772 phosphate is essential for the development of nasopharyngeal cancer.

Nasopharyngeal cancer (NPC) as a unique endemental distribution of head and neck cancer, the prevalence of the disease is very high in southern China and Southeast Asia, and is still one of the main fatal malignancies in these areas.
radiotherapy is a major treatment for NPC, however, since most NPC patients are terminally diagnosed with nonse specific symptoms, these patients exhibit poor radiotherapy results and prognostics.
explore the potential mechanisms for the development of NPC to better find new therapeutic targets for the disease.
EphA2 as a subject Tyrosine kinase (RTK) and is a member of the EphA family.
increasingly large number of studies have shown that EphA2, as an important target for carcinogenic proteins and emerging drugs, can promote/inhibit tumor development in a manner that is not dependent/dependent on the media.
previous studies have shown that 897th bit serine (S897) and 772nd tyrosine (Y772) of EphA2 are important phosphate residues.
Although numerous studies have shown that non-dependent S897 phosphate EphA2 (pS897-EphA2) can promote cancer development, it is not clear the carcinogenic effects and molecular mechanisms of non-dependent Y772 phosphate EphA2 (pY772-EphA2).
the study, the researchers used endoensothin EphA2 to remove nasopharyngeal cancer cells to build a stable cell line that over-expresses EphA2 and EphA2-Y772A (simulated dephosphorylation).
studies have shown that Y772 phosphateization of EphA2 is essential for the proliferation of EphA2-mediated NPC cells and the anchoring non-dependent growth of such cells in mice.
mechanism studies have shown that EphA2-Y772A in NPC cells can affect EphA2 activation of the Shp2/Erk-1/2 signal path, while Gab1 and Grb2 participate in the activation of pY772-EphA2.
further studies have shown that Shp2/Erk-1/2 signals regulate the proliferation and anchoring of non-dependent growth of pY772-EphA2-mediated NPC cells.
addition, EphA2-Y772A can weaken the inhibition effect of EphA2 inhibitor ALW-II-41-27 on pY772-EphA2, thereby reducing its inhibition of NPC cell proliferation.
in summary, the study showed that EphA2 protein 772th tyrosine phosphate is essential for the growth of EphA2-dependent nasopharyngeal cancer cells, a process achieved by activating the Shp2/Erk-1/2 signaling path.
and the point is a pharmacological target for ALW-II-41-27, indicating that pY772-EphA2 can be a potential therapeutic target for NPC and other cancers.
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