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S100A8通过自噬促进B细胞淋巴瘤耐药性的机制研究
引用本文:周仕霞,张力,李晓明,唐君玲.S100A8通过自噬促进B细胞淋巴瘤耐药性的机制研究[J].中国细胞生物学学报,2021(2):394-403.
作者姓名:周仕霞  张力  李晓明  唐君玲
作者单位:西南医科大学附属医院血液内科;西南医科大学附属医院干细胞实验室;西南医科大学口腔医学院口腔颌面外科
基金项目:四川省重点研发项目(批准号:2019YFS0301);四川省卫生健康委员会重点研究项目(批准号:18ZD014);泸州市科技局应用基础研究项目(批准号:2019LZXNYDJ54)资助的课题。
摘    要:B细胞淋巴瘤是起源于淋巴造血系统的恶性肿瘤,是由分化过程中淋巴细胞恶性转化的复杂过程引起的.B细胞淋巴瘤细胞的耐药性是制约B细胞淋巴瘤治疗的关键因素.自噬是细胞成分降解和再循环的重要细胞生物学过程,近年来其与肿瘤耐药性的相关性受到越来越多的关注.S100A8是钙结合蛋白S100家族的重要成员,其在淋巴瘤的的耐药调控中发...

关 键 词:B细胞淋巴瘤  耐药性  自噬  S100A8

S100A8 Promotes Chemoresistance of B-Cell Lymphoma via Autophagy
Authors:ZHOU Shixia  ZHANG Li  LI Xiaoming  TANG Junling
Institution:(Department of Hematology,Affiliated Hospital of Southwest Medical University,Luzhou 646000,China;Stem Cell Laboratory Affiliated to Southwest Medical University,Luzhou 646000,China;Department of Oraland Maxillofacial Surgery,Stomatological Hospital Affiliated to Southwest Medical University,Luzhou 646000,China)
Abstract:BCLs(B-cell lymphomas)are malignant tumors that originate from the lymphoid hematopoietic system,resulting from the complex process of malignant transformation of lymphocytes during various stages of differentiation.The efforts to control or even eradicate BCLs are frequently hampered by the development of drug resistance.Autophagy is a regulated process of degradation and recycling of cellular constituents,which recently received increasing attention for its roles in conferring resistance to various commonly used anticancer therapies.S100A8 is a member of the S100 calcium-binding protein family and plays an important role in the drug resistance of lymphoid tumors,while the mechanisms are particular unclear.In the present study,by employing three BCL cell lines(Daudi,SUDHL-4 and JeKo-1),S100A8 was found to be crucial in regulating drug resistance and activating autophagy in BCL cells.Interference of S100A8 could significantly down-regulate BNIP3 expression located in mitochondrial and endoplasmic reticulum to further inhibit autophagy.In addition,S100A8 interference notably inhibited the formation of BECN1-PI3KC3 complex and promoted BCL2 expression,which collectively inhibited autophagy.
Keywords:B-cell lymphomas  chemoresistance  autophagy  S100A8
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