LSR promotes epithelial ovarian cancer cell survival under energy stress through the LKB1-AMPK pathway.
AMP-Activated Protein Kinase Kinases
AMP-Activated Protein Kinases
/ metabolism
Carcinoma, Ovarian Epithelial
/ enzymology
Cell Line, Tumor
Cell Membrane
/ metabolism
Cell Proliferation
Cell Survival
Down-Regulation
Energy Metabolism
Enzyme Activation
Female
Glucose
/ deficiency
Humans
Protein Serine-Threonine Kinases
/ metabolism
Receptors, Lipoprotein
/ metabolism
Signal Transduction
Stress, Physiological
Transcription Factors
/ metabolism
Xenograft Model Antitumor Assays
AMPK
Cell survival
Energy stress
Epithelial ovarian cancer
LKB1
LSR
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
22 01 2021
22 01 2021
Historique:
received:
11
12
2020
revised:
14
12
2020
accepted:
22
12
2020
pubmed:
4
1
2021
medline:
23
4
2021
entrez:
3
1
2021
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 33388415
pii: S0006-291X(20)32261-0
doi: 10.1016/j.bbrc.2020.12.079
pii:
doi:
Substances chimiques
LSR protein, human
0
Receptors, Lipoprotein
0
Transcription Factors
0
Protein Serine-Threonine Kinases
EC 2.7.11.1
STK11 protein, human
EC 2.7.11.1
AMP-Activated Protein Kinase Kinases
EC 2.7.11.3
AMP-Activated Protein Kinases
EC 2.7.11.31
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
93-99Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
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.