(i) Tobacco smoke → upregulates EphA2 and downregulation of E-cadherin (1) Increased protein permeability via Erk1/Erk2, p54, and JNK-MAPK (ii) Highest EphA2 in patients who developed brain metastasis (iii) Constitutive activation via phosphorylation of pSer2448 and pSer2481 in MTOR (iv) Loss of EphA2→ loss of EGFR mutations in vitro in TKI resistant lung cancer cells (v) Phrenological inhibition of EphA2 via AWL-II-41-247 resulted in decreased proliferation of TKI resistant lung cancer cells (vi) Ephrin-B3 silencing→ stabilization of EphA2 via phosphorylation of Akt target Ser-897
(i) Upregulation of EphA3 → reduced PI3k/BMX/STAT3 signaling in SCLC cells → inducing G0/G1 arrest and increased apoptosis (ii) Ephrin-A3 coexpression inhibits EphA3 trans activation (1) Ephrin-A3 is 26x upregulated in NSCLC & absent in normal lung tissue
(i) EphA4 expression correlate with low stage and presence of inflammation (ii) Higher levels of EphA1, Eph4, EphA5, and EphA7 only present in nonadvance stages of lung cancer (E-COG performance score < 2)
(i) EphA7 expression correlate with older age, fibrosis, and smaller tumor size (ii) Higher levels of EphA1, Eph4, EphA5, and EphA7 only present in nonadvance stages of lung cancer (E-COG performance score < 2)
(i) Overexpression of EphB3→ accelerated cell growth and migration (ii) EphB3/Ephrin-B1→ decreased Akt activity via ternery formation of PP2A/RACK1/Akt (iii) EphB3 loss in vivo→ apoptosis due to increased activation of capase-8
(i) Silencing of ephrin-B3 in NSCLC line and stabilization of EphA2 via Akt target Ser-897 phosphorylation may promote stability of EphA2 in tumor survival