An ATG5 knockout promotes paclitaxel resistance in v-Ha-ras-transformed NIH 3T3 cells.
Animals
Antineoplastic Agents, Phytogenic
/ pharmacology
Apoptosis
/ drug effects
Autophagy
/ drug effects
Autophagy-Related Protein 5
/ genetics
CRISPR-Cas Systems
Cell Cycle
/ drug effects
Drug Resistance, Neoplasm
Gene Knockout Techniques
Genes, ras
Mice
NIH 3T3 Cells
Neoplasms
/ drug therapy
Paclitaxel
/ pharmacology
Tubulin Modulators
/ pharmacology
ATG5 knockout
Autophagy
Multi-drug resistance
Paclitaxel
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:
21 05 2019
21 05 2019
Historique:
received:
02
03
2019
accepted:
29
03
2019
pubmed:
8
4
2019
medline:
9
4
2020
entrez:
8
4
2019
Statut:
ppublish
Résumé
Autophagy plays a contradictory role in cell survival and death. Here, we investigated changes in paclitaxel sensitivity of cells with an ATG5 gene-knockout (KO), incapable of synthesizing an E3 ubiquitin ligase necessary for autophagy. The ATG5 KO in v-Ha-ras-transformed NIH 3T3 cells (Ras-NIH 3T3) was established using the CRISPR/Cas9 system. An LC3 immunoblot and a qRT-PCR assay were used to confirm the KO of functional ATG5. We found that the ATG5 KO led to paclitaxel resistance in Ras-NIH 3T3 cells through an ATP-binding cassette (ABC) transporter-independent mechanism. Flow cytometric analyses revealed that paclitaxel induced a remarkable significant G
Identifiants
pubmed: 30954217
pii: S0006-291X(19)30604-7
doi: 10.1016/j.bbrc.2019.03.197
pii:
doi:
Substances chimiques
Antineoplastic Agents, Phytogenic
0
Atg5 protein, mouse
0
Autophagy-Related Protein 5
0
Tubulin Modulators
0
Paclitaxel
P88XT4IS4D
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
234-241Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.