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作 者:Kenan Huang Biao Zhang Yu Feng Haitao Ma
机构地区:[1]Department of Thoracic Surgery,Dushu Lake Hospital Affiliated to Soochow University,Suzhou 215000,China [2]Department of Thoracic Surgery,Shanghai Changzheng Hospital,Navy Military Medical University,Shanghai 200003,China
出 处:《Acta Biochimica et Biophysica Sinica》2024年第7期1044-1054,共11页生物化学与生物物理学报(英文版)
基 金:supported by the grants from the Natural Science Foundation of Jiangsu Province(No.BK20191174);the Project of Shanghai Municipal Health Commission(No.202240394).
摘 要:Esophagus cancer(EC)is one of the most aggressive malignant digestive system tumors and has a high clinical incidence worldwide.Magnolol,a natural compound,has anticancer effects on many cancers,including esophageal carcinoma,but the underlying mechanism has not been fully elucidated.Here,we first find that magnolol inhibits the proliferation of esophageal carcinoma cells and enhances their autophagy activity in a dose-and time-dependent manner.This study demonstrates that magnolol increases the protein levels of LC3 II,accompanied by increased HACE1 protein levels in both esophageal carcinoma cells and xenograft tumors.HACE1-knockout(KO)cell lines are generated,and the ablation of HACE1 eliminates the anti-proliferative and autophagy-inducing effects of magnolol on esophageal carcinoma cells.Additionally,our results show that magnolol primarily promotes HACE1 expression at the transcriptional level.Therefore,this study shows that magnolol primarily exerts its antitumor effect by activating HACE1-OPTN axis-mediated autophagy.It can be considered a promising therapeutic drug for esophageal carcinoma.
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