{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T17:27:14Z","timestamp":1769189234622,"version":"3.49.0"},"reference-count":40,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2020,5,29]],"date-time":"2020-05-29T00:00:00Z","timestamp":1590710400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81770981"],"award-info":[{"award-number":["81770981"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>To explore the relationship between autophagy and cell function, we investigated how PLAC8\u2010mediated autophagy influences proliferation, apoptosis and epithelial\u2010mesenchymal transition (EMT) in NPC. Colony formation analyses and CCK8 assays were used to assess the proliferative capacity of NPC cells. Transmission electron microscopy (TEM) was used to identify autophagosomes. Autophagic flux was monitored using the tandem monomeric RFP\u2010GFP\u2010tagged LC3 (tfLC3) assay. The rate of apoptosis in NPC cells was analysed by flow cytometry. Western blot analysis was used to evaluate the activation of autophagy and the signalling status of the AKT\/mTOR pathway. Our study reveals that knocking out PLAC8 (koPLAC8) induces autophagy and apoptosis, while suppressing NPC cell proliferation and EMT. However, inhibition of autophagy with 3\u2010methyladenine or by knocking down Beclin\u20101 reverses the cell proliferation, apoptosis and EMT influenced by koPLAC8. We find that koPLAC8 inhibits the phosphorylation of AKT and its downstream target, mTOR. Moreover, immunofluorescence and co\u2010immunoprecipitation reveal complete PLAC8\/AKT colocalization and PLAC8\/AKT interaction, respectively. Furthermore, knockout of PLAC8 induced autophagy and inactivated AKT\/mTOR signalling pathway of NPC xenografts. Overall, our findings demonstrate that koPLAC8 induces autophagy via the AKT\/mTOR pathway, thereby inhibiting cell proliferation and EMT, and promoting apoptosis in NPC cells.<\/jats:p>","DOI":"10.1111\/jcmm.15409","type":"journal-article","created":{"date-parts":[[2020,5,29]],"date-time":"2020-05-29T07:32:14Z","timestamp":1590737534000},"page":"7778-7788","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Plac8\u2010mediated autophagy regulates nasopharyngeal carcinoma cell function via AKT\/mTOR pathway"],"prefix":"10.1111","volume":"24","author":[{"given":"Mao\u2010Ling","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Otolaryngology\u2010Head and Neck Surgery Central Laboratory Renmin Hospital of Wuhan University Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cheng\u2010Lin","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of 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