Document Detail

The effects on cell growth and chemosensitivity by livin RNAi in non-small cell lung cancer.
MedLine Citation:
PMID:  18827979     Owner:  NLM     Status:  MEDLINE    
Livin is highly expressed in most tumor tissues and could inhibit the tumor cells apoptosis. Knockdown of endogenous livin expression in non-small cell lung cancer (NSCLC) cells could inhibit cell growth. But it is still unclear if knockdown of endogenous livin expression combined with conventional chemotherapy could play a positive role in NSCLC treatment. In this article, the efficient RNA interferences (RNAi) of livin were constructed, and then we transfected them into A549 cells and 103H cells to study their influence on cell cycle and apoptosis index. At last, we detected the cell's sensitivity to conventional chemotherapeutic drugs after knockdown endogenous livin expression in A549 cells and 103H cells. Our results showed that knockdown livin expression could inhibit cell growth and induce apoptosis in A549 cells and 103H cells. A549 cells and 103H cells had an increased chemosensitivity to adriamycin and cisplatin after transfection of livin RNAi constructs. The results indicated that cell cycle redistribution and increased apoptosis index after knockdown livin expression might provide the main explanation for the enhanced chemosensitivity. Proper combination of livin RNAi and some conventional chemotherapeutic drugs may entail potential benefits in the treatment of NSCLC.
Dong Yuan; Liqun Liu; Huaming Xu; Dayong Gu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-10-01
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  320     ISSN:  1573-4919     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-10     Completed Date:  2009-11-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  133-40     Citation Subset:  IM    
Department of Thoracic Surgery, The Affiliated Hospital of Weifang Medical College, Weifang, China.
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MeSH Terms
Adaptor Proteins, Signal Transducing* / genetics,  metabolism
Antineoplastic Agents / therapeutic use*
Carcinoma, Non-Small-Cell Lung* / drug therapy,  metabolism
Cell Cycle / physiology
Cell Line
Dose-Response Relationship, Drug
Inhibitor of Apoptosis Proteins* / genetics,  metabolism
Inhibitory Concentration 50
Lung Neoplasms* / drug therapy,  metabolism
Neoplasm Proteins* / genetics,  metabolism
Protein Isoforms* / genetics,  metabolism
RNA Interference*
RNA, Small Interfering / genetics,  metabolism
Recombinant Fusion Proteins / genetics,  metabolism
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Antineoplastic Agents; 0/BIRC7 protein, human; 0/Inhibitor of Apoptosis Proteins; 0/Neoplasm Proteins; 0/Protein Isoforms; 0/RNA, Small Interfering; 0/Recombinant Fusion Proteins

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