schliessen

Filtern

 

Bibliotheken

Inhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells

Aim: The ubiquitin-proteasome system (UPS) and lysosome-dependent macroautophagy (autophagy) are two major intracellular pathways for protein degradation. Recent studies suggest that proteasome inhibitors may reduce tumor growth and activate autophagy. Due to the dual roles of autophagy in tumor cel... Full description

Journal Title: Acta pharmacologica Sinica 2009, Vol.30 (7), p.1046-1052
Main Author: Ge, Peng-Fei
Other Authors: Zhang, Ji-Zhou , Wang, Xiao-Fei , Meng, Fan-Kai , Li, Wen-Chen , Luan, Yong-Xin , Ling, Feng , Luo, Yi-Nan
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: Nature Publishing Group
ID: ISSN: 1671-4083
Link: https://www.ncbi.nlm.nih.gov/pubmed/19575007
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4006657
title: Inhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells
format: Article
creator:
  • Ge, Peng-Fei
  • Zhang, Ji-Zhou
  • Wang, Xiao-Fei
  • Meng, Fan-Kai
  • Li, Wen-Chen
  • Luan, Yong-Xin
  • Ling, Feng
  • Luo, Yi-Nan
subjects:
  • Animals
  • Apoptosis Regulatory Proteins - metabolism
  • autophagy
  • Autophagy - physiology
  • Beclin-1
  • Cell Cycle - physiology
  • cell death
  • Cell Death - physiology
  • Cell Line, Tumor - drug effects
  • Cysteine Proteinase Inhibitors - metabolism
  • Cysteine Proteinase Inhibitors - pharmacology
  • Glioma - metabolism
  • Glioma - pathology
  • Glioma - ultrastructure
  • Humans
  • Leupeptins - metabolism
  • Leupeptins - pharmacology
  • Membrane Proteins - metabolism
  • Microtubule-Associated Proteins - metabolism
  • Original
  • Original Article
  • Proteasome Endopeptidase Complex - metabolism
  • Proteasome Inhibitors
  • 抑制蛋白
  • 细胞死亡
  • 胶质瘤细胞
  • 酶抑制
ispartof: Acta pharmacologica Sinica, 2009, Vol.30 (7), p.1046-1052
description: Aim: The ubiquitin-proteasome system (UPS) and lysosome-dependent macroautophagy (autophagy) are two major intracellular pathways for protein degradation. Recent studies suggest that proteasome inhibitors may reduce tumor growth and activate autophagy. Due to the dual roles of autophagy in tumor cell survival and death, the effect of autophagy on the destiny of glioma cells remains unclear. In this study, we sought to investigate whether inhibition of the proteasome can induce autophagy and the effects of autophagy on the fate of human SHG-44 glioma cells. Methods: The proteasome inhibitor MG-132 was used to induce autophagy in SHG-44 glioma cells, and the effect of autophagy on the survival of SHG-44 glioma cells was investigated using an autophagy inhibitor 3-MA. Cell viability was measured by MTT assay. Apoptosis and cell cycle were detected by flow cytometry. The expression of autophagy related proteins was determined by Western blot. Results: MG-132 inhibited cell proliferation, induced cell death and cell cycle arrest at GJM phase, and activated autophagy in SHG-44 glioma cells. The expression of autophagy-related Beclin-1 and LC3-1 was significantly up-regulated and part of LC3-1 was converted into LC3-11. However, when SHG-44 glioma cells were co-treated with MG-132 and 3-MA, the cells became less viable, but cell death and cell numbers at G2/M phase increased. Moreover, the accumulation of acidic vesicular organelles was decreased, the expression of Beclin-1 and LC3 was significantly down-regulated and the conversion of LC3-11 from LC3-1 was also inhJbited. Conclusion: Inhibition of the proteasome can induce autophagy in human SHG-44 glioma cells, and inhibition of autophagy increases cell death. This discovery may shed new light on the effect of autophagy on modulating the fate of SHG-44 glioma cells.
language: eng
source:
identifier: ISSN: 1671-4083
fulltext: no_fulltext
issn:
  • 1671-4083
  • 1745-7254
url: Link


@attributes
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
RANK2.3440714
LOCALfalse
PrimoNMBib
record
control
sourceidproquest_pubme
recordidTN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4006657
sourceformatXML
sourcesystemPC
cqvip_id30813332
sourcerecordid20944650
originalsourceidFETCH-LOGICAL-1565t-a22b3a2d8cd09f82166110818530504aa0479f55fe4f6b650c6edbf82bed17670
addsrcrecordideNp9ks1v1DAQxSMEoqVw4g4RBzigLOPv5FIJVdCtVIkDcLYc20m8JHYaJ0j73-N0V6WtBCdb4988zTy_LHuNYIOAlJ_UGDcYoNoI9CQ7RYKyQmBGn6Y7F6igUJKT7EWMOwCCCaqeZyeoYoIBiNNsd-U7V7vZBZ-HJlfLHMZOtfvcebNoa_J6n49TmK2KYbCpekc7r6dUtTHXtu9zY9XcpWLeLYPy-fftZUFp3vYuDOqWiC-zZ43qo311PM-yn1-__LjYFtffLq8uPl8XiHE2FwrjmihsSm2gakqMOEcISlQyAgyoUkBF1TDWWNrwmjPQ3Jo6gbU1SHABZ9n5QXdc6sEabf08qV6OkxvUtJdBOfnwxbtOtuG3pACcs1VgexAIo_XKTfZBr_F2lsFIzIUklAtlUGm5wNgIXNUMSqsMpNE0B5OkPhxnmcLNYuMsBxdXN5S3YYlSEEI4EbRM5Pv_khgqStO2CXz3CNyFZfLJUYkRAcEEWVf4eID0FGKcbHO3AgK5pkam1Mg1NVKgRL-579hf9hiTBKBHctrNao1BMtD1_xB9e-jxal7ueZiYFbkljpvoLvj2xvlW1kr_alxvJUk_nrzB8AeMPeMA
sourcetypeOpen Access Repository
isCDItrue
recordtypearticle
pqid213075737
display
typearticle
titleInhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells
creatorGe, Peng-Fei ; Zhang, Ji-Zhou ; Wang, Xiao-Fei ; Meng, Fan-Kai ; Li, Wen-Chen ; Luan, Yong-Xin ; Ling, Feng ; Luo, Yi-Nan
creatorcontribGe, Peng-Fei ; Zhang, Ji-Zhou ; Wang, Xiao-Fei ; Meng, Fan-Kai ; Li, Wen-Chen ; Luan, Yong-Xin ; Ling, Feng ; Luo, Yi-Nan
descriptionAim: The ubiquitin-proteasome system (UPS) and lysosome-dependent macroautophagy (autophagy) are two major intracellular pathways for protein degradation. Recent studies suggest that proteasome inhibitors may reduce tumor growth and activate autophagy. Due to the dual roles of autophagy in tumor cell survival and death, the effect of autophagy on the destiny of glioma cells remains unclear. In this study, we sought to investigate whether inhibition of the proteasome can induce autophagy and the effects of autophagy on the fate of human SHG-44 glioma cells. Methods: The proteasome inhibitor MG-132 was used to induce autophagy in SHG-44 glioma cells, and the effect of autophagy on the survival of SHG-44 glioma cells was investigated using an autophagy inhibitor 3-MA. Cell viability was measured by MTT assay. Apoptosis and cell cycle were detected by flow cytometry. The expression of autophagy related proteins was determined by Western blot. Results: MG-132 inhibited cell proliferation, induced cell death and cell cycle arrest at GJM phase, and activated autophagy in SHG-44 glioma cells. The expression of autophagy-related Beclin-1 and LC3-1 was significantly up-regulated and part of LC3-1 was converted into LC3-11. However, when SHG-44 glioma cells were co-treated with MG-132 and 3-MA, the cells became less viable, but cell death and cell numbers at G2/M phase increased. Moreover, the accumulation of acidic vesicular organelles was decreased, the expression of Beclin-1 and LC3 was significantly down-regulated and the conversion of LC3-11 from LC3-1 was also inhJbited. Conclusion: Inhibition of the proteasome can induce autophagy in human SHG-44 glioma cells, and inhibition of autophagy increases cell death. This discovery may shed new light on the effect of autophagy on modulating the fate of SHG-44 glioma cells.
identifier
0ISSN: 1671-4083
1EISSN: 1745-7254
2DOI: 10.1038/aps.2009.71
3PMID: 19575007
languageeng
publisherUnited States: Nature Publishing Group
subjectAnimals ; Apoptosis Regulatory Proteins - metabolism ; autophagy ; Autophagy - physiology ; Beclin-1 ; Cell Cycle - physiology ; cell death ; Cell Death - physiology ; Cell Line, Tumor - drug effects ; Cysteine Proteinase Inhibitors - metabolism ; Cysteine Proteinase Inhibitors - pharmacology ; Glioma - metabolism ; Glioma - pathology ; Glioma - ultrastructure ; Humans ; Leupeptins - metabolism ; Leupeptins - pharmacology ; Membrane Proteins - metabolism ; Microtubule-Associated Proteins - metabolism ; Original ; Original Article ; Proteasome Endopeptidase Complex - metabolism ; Proteasome Inhibitors ; 抑制蛋白 ; 细胞死亡 ; 胶质瘤细胞 ; 酶抑制
ispartofActa pharmacologica Sinica, 2009, Vol.30 (7), p.1046-1052
rights
0Copyright Nature Publishing Group Jul 2009
1Copyright © 2009 CPS and SIMM 2009 CPS and SIMM
lds50peer_reviewed
oafree_for_read
citedbyFETCH-LOGICAL-1565t-a22b3a2d8cd09f82166110818530504aa0479f55fe4f6b650c6edbf82bed17670
citesFETCH-LOGICAL-1565t-a22b3a2d8cd09f82166110818530504aa0479f55fe4f6b650c6edbf82bed17670
links
openurl$$Topenurl_article
thumbnail$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg
backlink$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19575007$$D View this record in MEDLINE/PubMed
search
creatorcontrib
0Ge, Peng-Fei
1Zhang, Ji-Zhou
2Wang, Xiao-Fei
3Meng, Fan-Kai
4Li, Wen-Chen
5Luan, Yong-Xin
6Ling, Feng
7Luo, Yi-Nan
title
0Inhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells
1Acta pharmacologica Sinica
addtitleActa Pharmacologica Sinica
descriptionAim: The ubiquitin-proteasome system (UPS) and lysosome-dependent macroautophagy (autophagy) are two major intracellular pathways for protein degradation. Recent studies suggest that proteasome inhibitors may reduce tumor growth and activate autophagy. Due to the dual roles of autophagy in tumor cell survival and death, the effect of autophagy on the destiny of glioma cells remains unclear. In this study, we sought to investigate whether inhibition of the proteasome can induce autophagy and the effects of autophagy on the fate of human SHG-44 glioma cells. Methods: The proteasome inhibitor MG-132 was used to induce autophagy in SHG-44 glioma cells, and the effect of autophagy on the survival of SHG-44 glioma cells was investigated using an autophagy inhibitor 3-MA. Cell viability was measured by MTT assay. Apoptosis and cell cycle were detected by flow cytometry. The expression of autophagy related proteins was determined by Western blot. Results: MG-132 inhibited cell proliferation, induced cell death and cell cycle arrest at GJM phase, and activated autophagy in SHG-44 glioma cells. The expression of autophagy-related Beclin-1 and LC3-1 was significantly up-regulated and part of LC3-1 was converted into LC3-11. However, when SHG-44 glioma cells were co-treated with MG-132 and 3-MA, the cells became less viable, but cell death and cell numbers at G2/M phase increased. Moreover, the accumulation of acidic vesicular organelles was decreased, the expression of Beclin-1 and LC3 was significantly down-regulated and the conversion of LC3-11 from LC3-1 was also inhJbited. Conclusion: Inhibition of the proteasome can induce autophagy in human SHG-44 glioma cells, and inhibition of autophagy increases cell death. This discovery may shed new light on the effect of autophagy on modulating the fate of SHG-44 glioma cells.
subject
0Animals
1Apoptosis Regulatory Proteins - metabolism
2autophagy
3Autophagy - physiology
4Beclin-1
5Cell Cycle - physiology
6cell death
7Cell Death - physiology
8Cell Line, Tumor - drug effects
9Cysteine Proteinase Inhibitors - metabolism
10Cysteine Proteinase Inhibitors - pharmacology
11Glioma - metabolism
12Glioma - pathology
13Glioma - ultrastructure
14Humans
15Leupeptins - metabolism
16Leupeptins - pharmacology
17Membrane Proteins - metabolism
18Microtubule-Associated Proteins - metabolism
19Original
20Original Article
21Proteasome Endopeptidase Complex - metabolism
22Proteasome Inhibitors
23抑制蛋白
24细胞死亡
25胶质瘤细胞
26酶抑制
issn
01671-4083
11745-7254
fulltextfalse
rsrctypearticle
creationdate2009
recordtypearticle
recordideNp9ks1v1DAQxSMEoqVw4g4RBzigLOPv5FIJVdCtVIkDcLYc20m8JHYaJ0j73-N0V6WtBCdb4988zTy_LHuNYIOAlJ_UGDcYoNoI9CQ7RYKyQmBGn6Y7F6igUJKT7EWMOwCCCaqeZyeoYoIBiNNsd-U7V7vZBZ-HJlfLHMZOtfvcebNoa_J6n49TmK2KYbCpekc7r6dUtTHXtu9zY9XcpWLeLYPy-fftZUFp3vYuDOqWiC-zZ43qo311PM-yn1-__LjYFtffLq8uPl8XiHE2FwrjmihsSm2gakqMOEcISlQyAgyoUkBF1TDWWNrwmjPQ3Jo6gbU1SHABZ9n5QXdc6sEabf08qV6OkxvUtJdBOfnwxbtOtuG3pACcs1VgexAIo_XKTfZBr_F2lsFIzIUklAtlUGm5wNgIXNUMSqsMpNE0B5OkPhxnmcLNYuMsBxdXN5S3YYlSEEI4EbRM5Pv_khgqStO2CXz3CNyFZfLJUYkRAcEEWVf4eID0FGKcbHO3AgK5pkam1Mg1NVKgRL-579hf9hiTBKBHctrNao1BMtD1_xB9e-jxal7ueZiYFbkljpvoLvj2xvlW1kr_alxvJUk_nrzB8AeMPeMA
startdate2009
enddate2009
creator
0Ge, Peng-Fei
1Zhang, Ji-Zhou
2Wang, Xiao-Fei
3Meng, Fan-Kai
4Li, Wen-Chen
5Luan, Yong-Xin
6Ling, Feng
7Luo, Yi-Nan
generalNature Publishing Group
scope
02RA
192L
2CQIGP
3W94
4WU4
5~WA
6CGR
7CUY
8CVF
9ECM
10EIF
11NPM
12AAYXX
13CITATION
143V.
157QP
167QR
177T5
187TK
197TO
207U9
217X7
227XB
2388E
248FD
258FE
268FH
278FI
288FJ
298FK
30ABUWG
31AZQEC
32BBNVY
33BENPR
34BHPHI
35DWQXO
36FR3
37FYUFA
38GHDGH
39GNUQQ
40H94
41HCIFZ
42K9.
43LK8
44M0S
45M1P
46M7N
47M7P
48P64
49PQEST
50PQQKQ
51PQUKI
52PRINS
537X8
54BOBZL
55CLFQK
565PM
sort
creationdate2009
titleInhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells
authorGe, Peng-Fei ; Zhang, Ji-Zhou ; Wang, Xiao-Fei ; Meng, Fan-Kai ; Li, Wen-Chen ; Luan, Yong-Xin ; Ling, Feng ; Luo, Yi-Nan
facets
frbrtype5
frbrgroupidcdi_FETCH-LOGICAL-1565t-a22b3a2d8cd09f82166110818530504aa0479f55fe4f6b650c6edbf82bed17670
rsrctypearticles
prefilterarticles
languageeng
creationdate2009
topic
0Animals
1Apoptosis Regulatory Proteins - metabolism
2autophagy
3Autophagy - physiology
4Beclin-1
5Cell Cycle - physiology
6cell death
7Cell Death - physiology
8Cell Line, Tumor - drug effects
9Cysteine Proteinase Inhibitors - metabolism
10Cysteine Proteinase Inhibitors - pharmacology
11Glioma - metabolism
12Glioma - pathology
13Glioma - ultrastructure
14Humans
15Leupeptins - metabolism
16Leupeptins - pharmacology
17Membrane Proteins - metabolism
18Microtubule-Associated Proteins - metabolism
19Original
20Original Article
21Proteasome Endopeptidase Complex - metabolism
22Proteasome Inhibitors
23抑制蛋白
24细胞死亡
25胶质瘤细胞
26酶抑制
toplevelpeer_reviewed
creatorcontrib
0Ge, Peng-Fei
1Zhang, Ji-Zhou
2Wang, Xiao-Fei
3Meng, Fan-Kai
4Li, Wen-Chen
5Luan, Yong-Xin
6Ling, Feng
7Luo, Yi-Nan
collection
0中文科技期刊数据库
1中文科技期刊数据库-CALIS站点
2中文科技期刊数据库-7.0平台
3中文科技期刊数据库-自然科学
4中文科技期刊数据库-自然科学-生物科学
5中文科技期刊数据库- 镜像站点
6Medline
7MEDLINE
8MEDLINE (Ovid)
9MEDLINE
10MEDLINE
11PubMed
12CrossRef
13ProQuest Central (Corporate)
14Calcium & Calcified Tissue Abstracts
15Chemoreception Abstracts
16Immunology Abstracts
17Neurosciences Abstracts
18Oncogenes and Growth Factors Abstracts
19Virology and AIDS Abstracts
20Health & Medical Collection
21ProQuest Central (purchase pre-March 2016)
22Medical Database (Alumni Edition)
23Technology Research Database
24ProQuest SciTech Collection
25ProQuest Natural Science Collection
26Hospital Premium Collection
27Hospital Premium Collection (Alumni Edition)
28ProQuest Central (Alumni) (purchase pre-March 2016)
29ProQuest Central (Alumni Edition)
30ProQuest Central Essentials
31Biological Science Collection
32ProQuest Central
33Natural Science Collection
34ProQuest Central Korea
35Engineering Research Database
36Health Research Premium Collection
37Health Research Premium Collection (Alumni)
38ProQuest Central Student
39AIDS and Cancer Research Abstracts
40SciTech Premium Collection
41ProQuest Health & Medical Complete (Alumni)
42ProQuest Biological Science Collection
43Health & Medical Collection (Alumni Edition)
44Medical Database
45Algology Mycology and Protozoology Abstracts (Microbiology C)
46Biological Science Database
47Biotechnology and BioEngineering Abstracts
48ProQuest One Academic Eastern Edition
49ProQuest One Academic
50ProQuest One Academic UKI Edition
51ProQuest Central China
52MEDLINE - Academic
53OpenAIRE (Open Access)
54OpenAIRE
55PubMed Central (Full Participant titles)
jtitleActa pharmacologica Sinica
delivery
delcategoryRemote Search Resource
fulltextno_fulltext
addata
au
0Ge, Peng-Fei
1Zhang, Ji-Zhou
2Wang, Xiao-Fei
3Meng, Fan-Kai
4Li, Wen-Chen
5Luan, Yong-Xin
6Ling, Feng
7Luo, Yi-Nan
formatjournal
genrearticle
ristypeJOUR
atitleInhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells
jtitleActa pharmacologica Sinica
addtitleActa Pharmacologica Sinica
date2009
risdate2009
volume30
issue7
spage1046
epage1052
pages1046-1052
issn1671-4083
eissn1745-7254
notes
0Q786
1autophagy
2cell death
3proteasome inhibitors; autophagy; cell death
4Q251
5proteasome inhibitors
631-1347/R
7These authors contributed equally to this work.
abstractAim: The ubiquitin-proteasome system (UPS) and lysosome-dependent macroautophagy (autophagy) are two major intracellular pathways for protein degradation. Recent studies suggest that proteasome inhibitors may reduce tumor growth and activate autophagy. Due to the dual roles of autophagy in tumor cell survival and death, the effect of autophagy on the destiny of glioma cells remains unclear. In this study, we sought to investigate whether inhibition of the proteasome can induce autophagy and the effects of autophagy on the fate of human SHG-44 glioma cells. Methods: The proteasome inhibitor MG-132 was used to induce autophagy in SHG-44 glioma cells, and the effect of autophagy on the survival of SHG-44 glioma cells was investigated using an autophagy inhibitor 3-MA. Cell viability was measured by MTT assay. Apoptosis and cell cycle were detected by flow cytometry. The expression of autophagy related proteins was determined by Western blot. Results: MG-132 inhibited cell proliferation, induced cell death and cell cycle arrest at GJM phase, and activated autophagy in SHG-44 glioma cells. The expression of autophagy-related Beclin-1 and LC3-1 was significantly up-regulated and part of LC3-1 was converted into LC3-11. However, when SHG-44 glioma cells were co-treated with MG-132 and 3-MA, the cells became less viable, but cell death and cell numbers at G2/M phase increased. Moreover, the accumulation of acidic vesicular organelles was decreased, the expression of Beclin-1 and LC3 was significantly down-regulated and the conversion of LC3-11 from LC3-1 was also inhJbited. Conclusion: Inhibition of the proteasome can induce autophagy in human SHG-44 glioma cells, and inhibition of autophagy increases cell death. This discovery may shed new light on the effect of autophagy on modulating the fate of SHG-44 glioma cells.
copUnited States
pubNature Publishing Group
pmid19575007
doi10.1038/aps.2009.71
oafree_for_read