ArticleDrug design, development and therapy2018
Inhibiting eEF-2 kinase-mediated autophagy enhanced the cytocidal effect of AKT inhibitor on human nasopharyngeal carcinoma.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 14 citations in OpenAlex.
- Identification of a Novel Substrate for eEF2K and the AURKA-SOX8 as the Related Pathway in TNBC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Progress in the Development of Eukaryotic Elongation Factor 2 Kinase (eEF2K) Natural Product and Synthetic Small Molecule Inhibitors for Cancer Chemotherapy.International journal of molecular sciences · 2021Review
- Insights Into the Pathologic Roles and Regulation of Eukaryotic Elongation Factor-2 Kinase.Frontiers in molecular biosciences · 2021Review
- ELF-1 expression in nasopharyngeal carcinoma facilitates proliferation and metastasis of cancer cells via modulation of CCL2/CCR2 signaling.Cancer management and research · 2019Article
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9 authors at 1 institution in 1 country.
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Abstract
aimOur previous research showed that AKT inactivation via small molecule inhibitors did not induce significant apoptosis, but rather markedly increased autophagy in nasopharyngeal carcinoma (NPC). The purpose of the current study was to determine whether autophagy inhibition can enhance the anticancer efficacy of an AKT inhibitor (MK-2206). MATERIALS AND
methodsNPC cell lines CNE-2 (Epstein-Barr virus negative) and C666-1 (Epstein-Barr virus positive) were used to conduct the research. Autophagy induction effects were evaluated via Western blotting. Eukaryotic elongation factor-2 (eEF-2) kinase was specifically and stably knocked down using shRNA. The growth and proliferation of the cells were assessed by Cell Counting Kit-8. In CNE-2 xenograft tumors, the antitumor effects of an AKT inhibitor (MK-2206) combined with an eEF-2 kinase inhibitor (NH125) were tested.
resultsMK-2206 induced eEF-2 kinase-dependent autophagy in NPC cell lines. Knockdown of eEF-2 kinase using shRNA blunted the autophagy activated by MK-2206. Compared with treatment with MK-2206 alone, shRNA or NH125 suppressed eEF-2 kinase and increased the growth-inhibitory effect of MK-2206 on the human NPC cell lines. The synergistic effects of eEF-2 kinase inhibition and MK-2206 were similar to those of the combination of hydroxychloroquine and MK-2206. Moreover, NH125 showed good synergistic effects with MK-2206 in vivo.
conclusioneEF-2 kinase-mediated autophagy induced by AKT inhibition played a protective role in NPC cells. Inhibition of eEF-2 kinase may be an effective method for increasing the efficacy of an AKT inhibitor such as MK-2206 in NPC.
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