沉默PPAR-γ通过上调bcl-2表达抑制A549细胞凋亡

背景与目的肺癌耐药是肺癌患者死亡的主要原因,PPAR-γ可促进细胞凋亡,逆转肺癌耐药。本实验旨在探讨PPAR-γ表达下调对人肺癌A549顺铂耐受性和细胞凋亡的影响。方法构建siRNA沉默PPAR-γ的A549细胞系[A549/PPAR-γ（-）],应用MTT法检测顺铂对PPAR-γ沉默A549细胞增殖的影响,应用流式细胞术检测顺铂对PPAR-γ沉默A549细胞周期的影响,Western blot法检测磷酸化Akt（p-Akt）、caspase-3和bcl-2/bax的变化,最后以RT-PCR检测bcl-2的转录水平。结果成功构建出两个A549/PPAR-γ（-）细胞克隆,经RT-PCR和Wes...

Full description

Saved in:
Bibliographic Details
Published in中国肺癌杂志 Vol. 16; no. 3; pp. 125 - 130
Main Author 杨靖宇
Format Journal Article
LanguageChinese
Published 300051天津,天津胸科医院 2013
300070天津,天津医科大学研究生院
Subjects
bcl-2
PPAR-γ
细胞凋亡
肺肿瘤
细胞凋亡
bcl-2
肺肿瘤
PPAR-γ
Online AccessGet full text
ISSN1009-3419
1999-6187
DOI10.3779/j.issn.1009-3419.2013.03.02

Cover

Abstract 背景与目的肺癌耐药是肺癌患者死亡的主要原因,PPAR-γ可促进细胞凋亡,逆转肺癌耐药。本实验旨在探讨PPAR-γ表达下调对人肺癌A549顺铂耐受性和细胞凋亡的影响。方法构建siRNA沉默PPAR-γ的A549细胞系[A549/PPAR-γ（-）],应用MTT法检测顺铂对PPAR-γ沉默A549细胞增殖的影响,应用流式细胞术检测顺铂对PPAR-γ沉默A549细胞周期的影响,Western blot法检测磷酸化Akt（p-Akt）、caspase-3和bcl-2/bax的变化,最后以RT-PCR检测bcl-2的转录水平。结果成功构建出两个A549/PPAR-γ（-）细胞克隆,经RT-PCR和Western blot检测其PPAR-γ的水平明显下降。PPAR-γ沉默后,两个克隆A549细胞对顺铂的耐受性分别增加了1.29倍和1.60倍,肿瘤细胞的凋亡减少。Western blot检测显示Akt的磷酸化水平和bcl-2/bax水平升高,caspase-3表达降低,RT-PCR进一步显示bcl-2的转录水平升高。结论抑制A549中PPAR-γ的表达后,肿瘤细胞获得对顺铂药物更高的耐受性,其机制与升高Akt磷酸化水平和bcl-2表达水平,抑制细胞凋亡有关。PPAR-γ下调是临床肿瘤产生耐药性的可能机制之一。
AbstractList R734.2; 背景与目的 肺癌耐药是肺癌患者死亡的主要原因,PPAR-γ可促进细胞凋亡,逆转肺癌耐药.本实验旨在探讨PPAR-γ表达下调对人肺癌A549顺铂耐受性和细胞凋亡的影响.方法 构建siRNA沉默PPAR-γ的A549细胞系[A549/PPAR-γ(-)],应用MTT法检测顺铂对PPAR-γ沉默A549细胞增殖的影响,应用流式细胞术检测顺铂对PPAR-γ沉默A549细胞周期的影响,Western blot法检测磷酸化Akt(p-Akt)、caspase-3和bcl-2/bax的变化,最后以RT-PCR检测bcl-2的转录水平.结果 成功构建出两个A549/PPAR-γ(-)细胞克隆,经RT-PCR和Western blot检测其PPAR-γ的水平明显下降.PPAR-γ沉默后,两个克隆A549细胞对顺铂的耐受性分别增加了1.29倍和1.60倍,肿瘤细胞的凋亡减少.Western blot检测显示Akt的磷酸化水平和bcl-2/bax水平升高,caspase-3表达降低,RT-PCR进一步显示bcl-2的转录水平升高.结论 抑制A549中PPAR-γ的表达后,肿瘤细胞获得对顺铂药物更高的耐受性,其机制与升高Akt磷酸化水平和bcl-2表达水平,抑制细胞凋亡有关.PPAR-γ下调是临床肿瘤产生耐药性的可能机制之一.
背景与目的肺癌耐药是肺癌患者死亡的主要原因,PPAR-γ可促进细胞凋亡,逆转肺癌耐药。本实验旨在探讨PPAR-γ表达下调对人肺癌A549顺铂耐受性和细胞凋亡的影响。方法构建siRNA沉默PPAR-γ的A549细胞系[A549/PPAR-γ（-）],应用MTT法检测顺铂对PPAR-γ沉默A549细胞增殖的影响,应用流式细胞术检测顺铂对PPAR-γ沉默A549细胞周期的影响,Western blot法检测磷酸化Akt（p-Akt）、caspase-3和bcl-2/bax的变化,最后以RT-PCR检测bcl-2的转录水平。结果成功构建出两个A549/PPAR-γ（-）细胞克隆,经RT-PCR和Western blot检测其PPAR-γ的水平明显下降。PPAR-γ沉默后,两个克隆A549细胞对顺铂的耐受性分别增加了1.29倍和1.60倍,肿瘤细胞的凋亡减少。Western blot检测显示Akt的磷酸化水平和bcl-2/bax水平升高,caspase-3表达降低,RT-PCR进一步显示bcl-2的转录水平升高。结论抑制A549中PPAR-γ的表达后,肿瘤细胞获得对顺铂药物更高的耐受性,其机制与升高Akt磷酸化水平和bcl-2表达水平,抑制细胞凋亡有关。PPAR-γ下调是临床肿瘤产生耐药性的可能机制之一。
Author 杨靖宇
AuthorAffiliation 天津医科大学研究生院,天津300070 天津胸科医院,天津300051
AuthorAffiliation_xml – name: 300070天津,天津医科大学研究生院;300051天津,天津胸科医院
Author_FL Jingyu YANG
Author_FL_xml – sequence: 1
  fullname: Jingyu YANG
Author_xml – sequence: 1
  fullname: 杨靖宇
BookMark eNo1j81KAlEcxS9hkFoPES1a3el_v2bmthPpC4Qk3MvMnXtNsWs5ROQqELRs1S5aBO5aRkFEgr1BT6E2vkUTFhw4Z_HjHE4OZWzLaoQ2CDjM8-RWw6nHsXUIgMSME-lQIMyBVHQJZYmUErvE9zJp_kdWUC6OGwAulYxn0fbs5WY-ui-XC0f463V-9ZB89ifvg-S5G6ompsnwKRmPZ4O76fVbQXD5Peol3cdp_3byMVxFyyZoxnrtz_OosrtTKe7j0uHeQbFQwkr4FFNFiPAhlJoIEyhjZMR45FHjSqONiBTnmkhX8ihSYSgVZaAN4wyY9hjXwPJoc1F7EVgT2Fq10Tpv23Sw2qmZoNP5vQwMgKbk-oJUxy1bO6un7Gm7fhK0L6tcEMF9QdkPQZxoOA
ClassificationCodes R734.2
ContentType Journal Article
Copyright Copyright © Wanfang Data Co. Ltd. All Rights Reserved.
Copyright_xml – notice: Copyright © Wanfang Data Co. Ltd. All Rights Reserved.
DBID 2RA
92L
CQIGP
W91
~WA
2B.
4A8
92I
93N
PSX
TCJ
DOI 10.3779/j.issn.1009-3419.2013.03.02
DatabaseName 中文期刊服务平台
中文科技期刊数据库-CALIS站点
中文科技期刊数据库-7.0平台
中文科技期刊数据库-医药卫生
中文科技期刊数据库- 镜像站点
Wanfang Data Journals - Hong Kong
WANFANG Data Centre
Wanfang Data Journals
万方数据期刊 - 香港版
China Online Journals (COJ)
China Online Journals (COJ)
DatabaseTitleList

DeliveryMethod fulltext_linktorsrc
Discipline Medicine
DocumentTitleAlternate PPAR-γ Silencing Inhibits the Apoptosis of A549 Cells by Upregulating Bcl-2
DocumentTitle_FL PPAR-γ Silencing Inhibits the Apoptosis of A549 Cells by Upregulating Bcl-2
EISSN 1999-6187
EndPage 130
ExternalDocumentID zgfazz201303002
45154852
GroupedDBID ---
-05
04C
29R
2B.
2C~
2RA
2WC
3V.
5GY
5VS
6PF
92F
92I
92L
AAWTL
ABUWG
ACGFS
AFKRA
ALMA_UNASSIGNED_HOLDINGS
BENPR
BPHCQ
BVBZV
C1A
CCEZO
CCPQU
CIEJG
CQIGP
CW9
DIK
E3Z
EBD
EIHBH
EMOBN
EOJEC
F5P
GROUPED_DOAJ
HYE
IPNFZ
KQ8
KWQ
OBODZ
OK1
PIMPY
PQQKQ
PROAC
RIG
RNS
RPM
TCJ
TGQ
U1G
U5O
W91
~WA
4A8
93N
PGMZT
PHGZM
PHGZT
PMFND
PSX
ID FETCH-LOGICAL-c582-2c11580b9e15facff9d34d72f69fef5dc44e19694ddcbb9c230ef34303e734e03
ISSN 1009-3419
IngestDate Thu May 29 03:56:17 EDT 2025
Wed Feb 14 10:44:16 EST 2024
IsPeerReviewed true
IsScholarly true
Issue 3
Keywords 细胞凋亡
bcl-2
肺肿瘤
PPAR-γ
Language Chinese
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c582-2c11580b9e15facff9d34d72f69fef5dc44e19694ddcbb9c230ef34303e734e03
Notes PPAR-γ;Bcl-2;Apoptosis;Lung neoplasms
Background and objective Drug resistance is the one of primary causes of death in patients with lung cancer,PPAR-γ could induce the apoptosis and reverse drug resistance.The aim of this study is to investigate the expression of PPAR-γ on cisplatin sensitivity and apoptosis response of human lung cancer cell line A549.Methods Reconstruction of PPAR-γ silencing A549 cells（A549/PPAR-γ（-）） by siRNA.MTT assay was employed to determine the effect of cisplatin on the proliferation of A549/PPAR-γ（-）,flow cytometry to determine the effect of cisplatin on the cell apoptosis,Western blot to determine the change of phosphorylation of Akt,caspase-3 and expression of bcl-2/bax.Finally,RT-PCR was employed to determine the transcriptional level of bcl-2.Results Two PPAR-γ silencing A549 cell clones were established successfully,and the expression of PPAR-γ was downregulated significantly as confirmed by RT-PCR and Western blot.After PPAR-γ silencing,the resistance of these two A549 clones
PageCount 6
ParticipantIDs wanfang_journals_zgfazz201303002
chongqing_primary_45154852
PublicationCentury 2000
PublicationDate 2013
PublicationDateYYYYMMDD 2013-01-01
PublicationDate_xml – year: 2013
  text: 2013
PublicationDecade 2010
PublicationTitle 中国肺癌杂志
PublicationTitleAlternate Chinese Journal of Lung Cancer
PublicationTitle_FL Chinese Journal of Lung Cancer
PublicationYear 2013
Publisher 300051天津,天津胸科医院
300070天津,天津医科大学研究生院
Publisher_xml – name: 300070天津,天津医科大学研究生院
– name: 300051天津,天津胸科医院
SSID ssj0062934
ssib002262905
ssib044765436
ssib001103766
ssib038074678
ssib051369142
Score 1.9558723
Snippet 背景与目的肺癌耐药是肺癌患者死亡的主要原因,PPAR-γ可促进细胞凋亡,逆转肺癌耐药。本实验旨在探讨PPAR-γ表达下调对人肺癌A549顺铂耐受性和细胞凋亡的影响。方法构建siRNA沉...
R734.2; 背景与目的 肺癌耐药是肺癌患者死亡的主要原因,PPAR-γ可促进细胞凋亡,逆转肺癌耐药.本实验旨在探讨PPAR-γ表达下调对人肺癌A549顺铂耐受性和细胞凋亡的影响.方法 ...
SourceID wanfang
chongqing
SourceType Aggregation Database
Publisher
StartPage 125
SubjectTerms bcl-2
PPAR-γ
细胞凋亡
肺肿瘤
Title 沉默PPAR-γ通过上调bcl-2表达抑制A549细胞凋亡
URI http://lib.cqvip.com/qk/91098A/201303/45154852.html
https://d.wanfangdata.com.cn/periodical/zgfazz201303002
Volume 16
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVAFT
  databaseName: Open Access Digital Library
  customDbUrl:
  eissn: 1999-6187
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0062934
  issn: 1009-3419
  databaseCode: KQ8
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html
  providerName: Colorado Alliance of Research Libraries
– providerCode: PRVAON
  databaseName: DOAJ Directory of Open Access Journals
  customDbUrl:
  eissn: 1999-6187
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0062934
  issn: 1009-3419
  databaseCode: DOA
  dateStart: 20080101
  isFulltext: true
  titleUrlDefault: https://www.doaj.org/
  providerName: Directory of Open Access Journals
– providerCode: PRVBFR
  databaseName: Free Medical Journals
  customDbUrl:
  eissn: 1999-6187
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0062934
  issn: 1009-3419
  databaseCode: DIK
  dateStart: 19980101
  isFulltext: true
  titleUrlDefault: http://www.freemedicaljournals.com
  providerName: Flying Publisher
– providerCode: PRVHPJ
  databaseName: ROAD: Directory of Open Access Scholarly Resources
  customDbUrl:
  eissn: 1999-6187
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssib044765436
  issn: 1009-3419
  databaseCode: M~E
  dateStart: 19980101
  isFulltext: true
  titleUrlDefault: https://road.issn.org
  providerName: ISSN International Centre
– providerCode: PRVAQN
  databaseName: PubMed Central
  customDbUrl:
  eissn: 1999-6187
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0062934
  issn: 1009-3419
  databaseCode: RPM
  dateStart: 20100101
  isFulltext: true
  titleUrlDefault: https://www.ncbi.nlm.nih.gov/pmc/
  providerName: National Library of Medicine
– providerCode: PRVPQU
  databaseName: East & South Asia Database
  customDbUrl:
  eissn: 1999-6187
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0062934
  issn: 1009-3419
  databaseCode: BVBZV
  dateStart: 19980101
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/eastsouthasia
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: ProQuest Central
  customDbUrl: http://www.proquest.com/pqcentral?accountid=15518
  eissn: 1999-6187
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0062934
  issn: 1009-3419
  databaseCode: BENPR
  dateStart: 19980101
  isFulltext: true
  titleUrlDefault: https://www.proquest.com/central
  providerName: ProQuest
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnR1Na9RAdFhaKF7ET2zVsqBzTN1MJsmMt2R3ShFalrJCb0sySbYH2VbdXvYkFqzWkzfxIPTmURRELNR_4K9o6_Zf-N5kNruIFBWWkLy8mXnkvX0fk_deCLmLIUGos8xxEx8CFF0wJ2FJ6GhszJJ7TIemin91LVh5yB9s-Bu12vOprKWdQbqkh3-sK_kfrgIM-IpVsv_A2WpSAMA58BeOwGE4_hWPqQpozKiQVEkax1SKdjtad2hT0dhDGKYxRFQJGi9TiPoVp7GgooQ0qPBS_chheBW5NBIGrPAH8wKWdKnyqQBgEEGAR1WIi4gA8YRHpTK3QypiM3MEs0z7una5qIVoMqZxywxkiAlTSSCviSvJFgIBB4iUlVm0d5AqiScyQJRIUWs57U5FWWJq1Sq-gsHOcaXVKWHY_yBw7aCxLg6mZM6bUqxuWR5tbbRbvsv5Xf1j80Sj_nGBpWpRTODzTCtbNrF6VS4i9zFq88GMzzLc05khs7Faa69PnEospZwOclnA5ERLYsd-sDaVFuM8xHrdCt93PRB7XjU1g8FlrsOYvDlyx9J-7xzKsffH5la_9xg8GlNg1i-Sfm_KF-pcIhdtEFOPSom8TGrDzStkbtWmaVwl908_vTo7fGuE8cfns2fvRt_3jr_ujz7uGoEbHXwYHR2d7r85efkFBevn4YvR7vuTvdfH3w6ukc6y6jRXHPuRDkf7EJwxDSGFaKQyd_0i0UUhM49nISsCWeSFn2nOc-zAxLNMp6nUEPHmhcfBccpDj-cN7zqZ6W_18xuknqVJJn3tweiUJ6lMuA5Y6MpcZn4eMD1PFqon0N0ue7F0x9ybJ3X7SLr2D_q0O-wVyXCIjxAsWYMtnDf-JrnAzIdOcHPtFpkZPNnJb4O7OUgXrTwsmu2aX0MZZHM
linkProvider ProQuest
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=%E6%B2%89%E9%BB%98PPAR-%CE%B3%E9%80%9A%E8%BF%87%E4%B8%8A%E8%B0%83bcl-2%E8%A1%A8%E8%BE%BE%E6%8A%91%E5%88%B6A549%E7%BB%86%E8%83%9E%E5%87%8B%E4%BA%A1&rft.jtitle=%E4%B8%AD%E5%9B%BD%E8%82%BA%E7%99%8C%E6%9D%82%E5%BF%97&rft.au=%E6%9D%A8%E9%9D%96%E5%AE%87&rft.date=2013&rft.issn=1009-3419&rft.eissn=1999-6187&rft.volume=16&rft.issue=3&rft.spage=125&rft.epage=130&rft_id=info:doi/10.3779%2Fj.issn.1009-3419.2013.03.02&rft.externalDocID=45154852
thumbnail_s http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=http%3A%2F%2Fimage.cqvip.com%2Fvip1000%2Fqk%2F91098A%2F91098A.jpg
http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=http%3A%2F%2Fwww.wanfangdata.com.cn%2Fimages%2FPeriodicalImages%2Fzgfazz%2Fzgfazz.jpg