Inhibition of PI3K-Akt pathway reverses LMP1 induced TRAIL resistance in nasopharyngeal carcinoma cell

Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery
S S LiP Li

Abstract

Objective:To observe the role of PI3K-Akt pathway in epsterin barr virus latent membrane protein 1(LMP1) induced TNF-related apoptosis inducing ligand(TRAIL) resistance in nasopharyngeal carcinoma(NPC) cell. Method:Expressions of Akt and p-Akt were detected after LMP1 overexpression by western blot. Colocation of LMP1 and p-Akt was detected by immunofluorescence. PI3K-Akt pathway was inhibited by LY294002 in CNE 1 and CNE 1+ LMP1. Then TRAIL sensitivity of CNE 1+ LMP1 and CNE 1 was analyzed by MTT and flow cytometric analysis, respectively. Activation of cell extrinsic apoptotic pathway was analyzed by western blot. Result:The expression of p-Akt in CNE 1+ LMP1 was higher than CNE 1. Immunofluorescence showed that after LMP1 overexpression in CNE 1, p-Akt was translocated from cytoplasm to membrane. With 1 μmol/ml LY294002 pretreatment for 8 hours, p-Akt expression was both downregulated in CNE 1 and CNE 1+ LMP1, but there was no significant difference between them(P >0.05). Moreover, the cytotoxicity and apoptosis induced by TRAIL in CNE 1 were enhanced after LMP1 overexpression and there was no significant difference between CNE 1 and CNE 1+ LMP1(P >0.05). Conclusion:LMP1 induced TRAIL-resistance in NPC cell through activetin...Continue Reading

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