Document Detail

Inhibitor of growth 4 induces apoptosis in human lung adenocarcinoma cell line A549 via Bcl-2 family proteins and mitochondria apoptosis pathway.
MedLine Citation:
PMID:  19034511     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Inhibitor of growth 4 (ING4) is considered to be a tumor suppressor implicated in several human malignancies by tumor growth inhibition and apoptosis enhancement. In present study, the effects of ING4 on apoptosis and its mechanisms were investigated through the transduction of ING4 cDNA into lung adenocarcinoma cell line A549. METHODS: The effects of ING4 on A549 apoptosis were observed by FCM analysis, TUNEL assay, and electron microscopy. Simultaneously, the effects of ING4 on the expression of several apoptosis-related proteins in cell line A549 were evaluated by Western blot analysis. RESULTS: Both Annexin-V FITC analysis by FCM and TUNEL assay revealed more apoptotic cells in A549 cells with exogenous ING4 gene. For electron microscopy, A549 cells with exogenous ING4 gene showed typical morphological changes of apoptosis. The deregulation of Bcl-2 family proteins (Bcl-2, Bcl-xl, Bax, Bak, Bid) and the major apoptotic executioners of mitochondria pathway (Cyt-c, caspase3, PARP) were also observed. CONCLUSION: Our findings suggest that exogenous ING4 can enhance A549 apoptosis via regulating the expression of Bcl-2 family proteins and the activation of mitochondrial apoptotic pathway.
Xiaomei Li; Qingyuan Zhang; Limin Cai; Yanhua Wang; Qian Wang; Xiaoyi Huang; Songbin Fu; Jing Bai; Jinglei Liu; Guangmei Zhang; Jiping Qi
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-11-26
Journal Detail:
Title:  Journal of cancer research and clinical oncology     Volume:  135     ISSN:  1432-1335     ISO Abbreviation:  J. Cancer Res. Clin. Oncol.     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-04-30     Completed Date:  2009-05-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7902060     Medline TA:  J Cancer Res Clin Oncol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  829-35     Citation Subset:  IM    
Department of Pathology, The Affiliated Tumor Hospital of Harbin Medical University, Harbin 150040, China.
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MeSH Terms
Adenocarcinoma / metabolism,  pathology,  physiopathology*
Apoptosis / physiology*
Blotting, Western
Caspase 3 / metabolism
Cell Cycle Proteins / genetics,  metabolism,  physiology*
Cell Line, Tumor
Cytochromes c / metabolism
Flow Cytometry
Homeodomain Proteins / genetics,  metabolism,  physiology*
In Situ Nick-End Labeling
Lung / metabolism,  pathology,  ultrastructure
Lung Neoplasms / metabolism,  pathology,  physiopathology*
Mice, Inbred BALB C
Mice, Nude
Microscopy, Electron
Mitochondria / metabolism*
Neoplasm Transplantation
Proto-Oncogene Proteins c-bcl-2 / metabolism*
Signal Transduction / physiology
Transplantation, Heterologous
Tumor Suppressor Proteins / genetics,  metabolism,  physiology*
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Homeodomain Proteins; 0/ING4 protein, human; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Suppressor Proteins; 9007-43-6/Cytochromes c; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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