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LSR promotes epithelial ovarian cancer cell survival under energy stress through the LKB1-AMPK pathway.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2021 Jan 22; Vol. 537, pp. 93-99. Date of Electronic Publication: 2020 Dec 31. - Publication Year :
- 2021
-
Abstract
- Lipolysis-stimulated lipoprotein receptor (LSR), also known as a component of tricellular tight junctions, is highly expressing in epithelial ovarian cancer (EOC). However, the biological role of LSR in EOC cells remains unclear. In this study, we evaluated liver kinase B1 (LKB1) mediated AMP-activated protein kinase (AMPK) activity and investigated the effect of LSR on EOC cell survival under energy stress. LSR increased the levels of phospho-AMPKα at Thr172 and phospho-acetyl-CoA carboxylase (ACC) at Ser79 via LKB1-AMPK pathway in glucose deprivation in vitro. The increase of P-AMPKα (Thr172) and P-ACC (Ser79) was also detected in tumor microenvironment in vivo. Meanwhile, LSR promoted LKB1 localization at the cell membrane of EOC cells. By cell survival analysis, LSR attenuated glucose deprivation-induced cell death in EOC cells in vitro. Our results suggest that LSR promotes EOC cell survival and tumor growth through the LKB1-AMPK pathway.<br />Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2020 Elsevier Inc. All rights reserved.)
- Subjects :
- AMP-Activated Protein Kinase Kinases
Cell Line, Tumor
Cell Membrane metabolism
Cell Proliferation
Cell Survival
Down-Regulation
Enzyme Activation
Female
Glucose deficiency
Humans
Signal Transduction
Xenograft Model Antitumor Assays
AMP-Activated Protein Kinases metabolism
Carcinoma, Ovarian Epithelial enzymology
Carcinoma, Ovarian Epithelial pathology
Energy Metabolism
Protein Serine-Threonine Kinases metabolism
Receptors, Lipoprotein metabolism
Stress, Physiological
Transcription Factors metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 537
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 33388415
- Full Text :
- https://doi.org/10.1016/j.bbrc.2020.12.079