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Tytuł pozycji:

Gamabufotalin induces a negative feedback loop connecting ATP1A3 expression and the AQP4 pathway to promote temozolomide sensitivity in glioblastoma cells by targeting the amino acid Thr794.

Tytuł:
Gamabufotalin induces a negative feedback loop connecting ATP1A3 expression and the AQP4 pathway to promote temozolomide sensitivity in glioblastoma cells by targeting the amino acid Thr794.
Autorzy:
Lan YL; Department of Neurosurgery, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern, University of Science and Technology, Shenzhen, China.; Department of Neurosurgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.; Department of Physiology, Dalian Medical University, Dalian, China.
Chen C; Department of Neurosurgery, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern, University of Science and Technology, Shenzhen, China.
Wang X; Department of Neurosurgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Lou JC; Department of Neurosurgery, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern, University of Science and Technology, Shenzhen, China.; Department of Neurosurgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Xing JS; Department of Neurosurgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Zou S; Department of Physiology, Dalian Medical University, Dalian, China.
Hu JL; Department of Neurosurgery, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern, University of Science and Technology, Shenzhen, China.
Lyu W; Department of Neurosurgery, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern, University of Science and Technology, Shenzhen, China.
Zhang B; Department of Neurosurgery, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern, University of Science and Technology, Shenzhen, China.; Department of Neurosurgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Źródło:
Cell proliferation [Cell Prolif] 2020 Jan; Vol. 53 (1), pp. e12732. Date of Electronic Publication: 2019 Nov 20.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: [Oxford, England] : Published for the Cell Kinetics Society, the European Study Group for Cell Proliferation, and the International Cell Cycle Society by Blackwell Scientific Publications, 1991-
MeSH Terms:
Aquaporin 4/*metabolism
Bufanolides/*pharmacology
Drug Resistance, Neoplasm/*drug effects
Gene Expression Regulation, Enzymologic/*drug effects
Gene Expression Regulation, Neoplastic/*drug effects
Glioblastoma/*drug therapy
Neoplasm Proteins/*biosynthesis
Sodium-Potassium-Exchanging ATPase/*biosynthesis
Temozolomide/*pharmacology
Animals ; Aquaporin 4/genetics ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Mice ; Neoplasm Proteins/genetics ; Sodium-Potassium-Exchanging ATPase/genetics ; Xenograft Model Antitumor Assays
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Grant Information:
2015002 Distinguished Professor Project of Liaoning Province, Special Grant for Translational Medicine, Dalian Medical University; LQ2017033 Basic research projects in colleges and universities of Liaoning Province; LR2016023 Liaoning province innovation talents support program in Colleges and Universities; 81372714 National Natural Science Foundation of China; 81672480 National Natural Science Foundation of China; 81802506 National Natural Science Foundation of China; 81872065 National Natural Science Foundation of China; 201602244 Natural Science Foundation of Liaoning Province
Contributed Indexing:
Keywords: AQP4; ATP1A3; gamabufotalin; glioblastoma multiforme; temozolomide
Substance Nomenclature:
0 (AQP4 protein, human)
0 (ATP1A3 protein, human)
0 (Aquaporin 4)
0 (Bufanolides)
0 (Neoplasm Proteins)
5HH3KM165O (gamabufotalin)
EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
YF1K15M17Y (Temozolomide)
Entry Date(s):
Date Created: 20191121 Date Completed: 20200225 Latest Revision: 20210110
Update Code:
20240104
PubMed Central ID:
PMC6985666
DOI:
10.1111/cpr.12732
PMID:
31746080
Czasopismo naukowe
Objectives: Temozolomide (TMZ) is one of the most commonly used clinical drugs for glioblastoma (GBM) treatment, but its drug sensitivity needs to be improved. Gamabufotalin (CS-6), the primary component of the traditional Chinese medicine "ChanSu," was shown to have strong anti-cancer activity. However, more efforts should be directed towards reducing its toxicity or effective treatment doses.
Methods: Target fishing experiment, Western blotting, PCR, confocal immunofluorescence and molecular cloning techniques were performed to search for possible downstream signalling pathways. In addition, GBM xenografts were used to further determine the potential molecular mechanisms of the synergistic effects of CS-6 and TMZ in vivo.
Results: Mechanistic research revealed a negative feedback loop between ATP1A3 and AQP4 through which CS-6 inhibited GBM growth and mediated the synergistic treatment effect of CS-6 and TMZ. In addition, by mutating potential amino acid residues of ATP1A3, which were predicted by modelling and docking to interact with CS-6, we demonstrated that abrogating hydrogen bonding of the amino acid Thr794 interferes with the activation of ATP1A3 by CS-6 and that the Thr794Ala mutation directly affects the synergistic treatment efficacy of CS-6 and TMZ.
Conclusions: As the main potential target of CS-6, ATP1A3 activation critically depends on the hydrogen bonding of Thr794 with CS-6. The combination of CS-6 and TMZ could significantly reduce the therapeutic doses and promote the anti-cancer efficacy of CS-6/TMZ monotherapy.
(© 2019 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.)

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