LncRP11-675F6.3 responds to rapamycin treatment and reduces triglyceride accumulation via interacting with HK1 in hepatocytes by regulating autophagy and VLDL-related proteins

doi:10.3724/abbs.2023091

科研成果详情

题名	LncRP11-675F6.3 responds to rapamycin treatment and reduces triglyceride accumulation via interacting with HK1 in hepatocytes by regulating autophagy and VLDL-related proteins
作者	Wang, Lingling1; Fang, Xiaojuan1; Yang, Ziyou1; Li, Xueling1; Cheng, Mengdi1; Cheng, Liang1; Wang, Ganglin1; Li, Wei1; Liu, Lin1,2
发表日期	2023-10
发表期刊	Acta biochimica et biophysica Sinica 影响因子和分区
语种	英语
原始文献类型	Journal Article
关键词	autophagy hexokinase 1 lipoprotein lncRP11-675F6.3 nonalcoholic fatty liver disease triglycerides
其他关键词	LONG NONCODING RNA ; METABOLISM ; GLUCOSE
摘要	Long noncoding RNAs (lncRNAs) have been widely proven to be involved in liver lipid homeostasis. Herein, we identify an upregulated lncRNA named lncRP11-675F6.3 in response to rapamycin treatment using a microarray in HepG2 cells. Knockdown of lncRP11-675F6. 3 leads to a significant reduction in apolipoprotein 100 (ApoB100), microsomal triglyceride transfer protein (MTTP), ApoE and ApoC3 with increased cellular triglyceride level and autophagy. Furthermore, we find that ApoB100 is obviously colocalized with GFP-LC3 in autophagosomes when lncRP11-675F6. 3 is knocked down, indicating that elevated triglyceride accumulation likely related to autophagy induces the degradation of ApoB100 and impairs very low-density lipoprotein (VLDL) assembly. We then identify and validate that hexokinase 1 (HK1) acts as the binding protein of lncRP11-675F6.3 and mediates triglyceride regulation and cell autophagy. More importantly, we find that lncRP11-675F6.3 and HK1 attenuate high fat diet induced nonalcoholic fatty liver disease (NAFLD) by regulating VLDL-related proteins and autophagy. In conclusion, this study reveals that lncRP11-675F6.3 is potentially involved in the downstream of mTOR signaling pathway and the regulatory network of hepatic triglyceride metabolism in cooperation with its interacting protein HK1, which may provide a new target for fatty liver disorder treatment
资助项目	National Natural Science Foundation of China [81970753]; Wenzhou Science and Technology Bureau Foundation [ZY2021011]
出版者	SCIENCE PRESS
ISSN	1672-9145
EISSN	1745-7270
卷号	55 期号:10 页码:1606-1617
DOI	10.3724/abbs.2023091
页数	12
WOS类目	Biochemistry & Molecular Biology ; Biophysics
WOS研究方向	Biochemistry & Molecular Biology ; Biophysics
WOS记录号	WOS:001087272900008
收录类别	PUBMED ; SCIE ; SCOPUS
URL	查看原文
PubMed ID	37222534
SCOPUSEID	2-s2.0-85174752135
通讯作者地址	[Li, Wei]Key Laboratory of Laboratory Medicine,Ministry of Education of China,Zhejiang Provincial Key Laboratory of Medical Genetics,School of Laboratory Medicine and Life Sciences,Wenzhou Medical University,Wenzhou,325035,China ; [Liu, Lin]Key Laboratory of Laboratory Medicine,Ministry of Education of China,Zhejiang Provincial Key Laboratory of Medical Genetics,School of Laboratory Medicine and Life Sciences,Wenzhou Medical University,Wenzhou,325035,China
Scopus学科分类	Biophysics;Biochemistry;Molecular Biology
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/180557
专题	检验医学院（生命科学学院、生物学实验教学中心）其他_附属诸暨医院（诸暨市人民医院）
通讯作者	Li, Wei; Liu, Lin
作者单位	1.Key Laboratory of Laboratory Medicine,Ministry of Education of China,Zhejiang Provincial Key Laboratory of Medical Genetics,School of Laboratory Medicine and Life Sciences,Wenzhou Medical University,Wenzhou,325035,China; 2.Zhuji Affiliated Hospital of Wenzhou Medical University,Shaoxing,311800,China
第一作者单位	检验医学院（生命科学学院、生物学实验教学中心）
通讯作者单位	检验医学院（生命科学学院、生物学实验教学中心）
第一作者的第一单位	检验医学院（生命科学学院、生物学实验教学中心）
推荐引用方式 GB/T 7714	Wang, Lingling,Fang, Xiaojuan,Yang, Ziyou,et al. LncRP11-675F6.3 responds to rapamycin treatment and reduces triglyceride accumulation via interacting with HK1 in hepatocytes by regulating autophagy and VLDL-related proteins[J]. Acta biochimica et biophysica Sinica,2023,55(10):1606-1617.
APA	Wang, Lingling., Fang, Xiaojuan., Yang, Ziyou., Li, Xueling., Cheng, Mengdi., ... & Liu, Lin. (2023). LncRP11-675F6.3 responds to rapamycin treatment and reduces triglyceride accumulation via interacting with HK1 in hepatocytes by regulating autophagy and VLDL-related proteins. Acta biochimica et biophysica Sinica, 55(10), 1606-1617.
MLA	Wang, Lingling,et al."LncRP11-675F6.3 responds to rapamycin treatment and reduces triglyceride accumulation via interacting with HK1 in hepatocytes by regulating autophagy and VLDL-related proteins".Acta biochimica et biophysica Sinica 55.10(2023):1606-1617.