Document Detail

MicroRNA-34a is an important component of PRIMA-1-induced apoptotic network in human lung cancer cells.
MedLine Citation:
PMID:  19921694     Owner:  NLM     Status:  MEDLINE    
Restoration of p53 function in tumor cells would be an attractive strategy for lung cancer therapy because p53 mutations are found in more than 50% of lung cancers. The small molecule PRIMA-1 has been shown to restore the tumor suppression function of p53 and to induce apoptosis in human tumor cells. The mechanism of apoptosis induced by PRIMA-1 remains unclear. We investigated the effects of PRIMA-1 in apoptosis with Western immunoblot analysis, TaqMan microRNA real-time PCR, cell viability analysis and flow cytometry using human lung cancer cell lines containing mutant (H211 and H1155), wild-type (A549) or null (H1299) p53. PRIMA-1 induced massive apoptosis in the H211 and H1155 cells, but was less toxic to the A549 and H1299 cells. Western immunoblot analysis showed cleavage of PARP in H211 and H1155 cells but not in A549 and H1299 cells following treatment with PRIMA-1. In addition, p53 protein was also phosphorylated in H211 and H1155 cells. TaqMan microRNA assay showed that the expression of microRNA-34a was increased in the H211 and H1155 cells posttreatment. Knockdown microRNA-34a decreased the rate of apoptosis caused by PRIMA-1. The above results suggest that microRNA-34a is one of the important components of PRIMA-1-induced apoptotic network in the cancer cells harboring mutant p53.
Wenrui Duan; Li Gao; Xin Wu; Li Wang; Serge P Nana-Sinkam; Gregory A Otterson; Miguel A Villalona-Calero
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  127     ISSN:  1097-0215     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-05-26     Completed Date:  2010-06-22     Revised Date:  2014-09-07    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  313-20     Citation Subset:  IM    
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MeSH Terms
Blotting, Western
Cell Proliferation
Lung Neoplasms / genetics*,  metabolism,  pathology*
Membrane Proteins / physiology*
MicroRNAs / physiology*
Mutation / genetics
Nerve Tissue Proteins / physiology*
RNA, Messenger / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Tumor Suppressor Protein p53 / genetics,  metabolism
Grant Support
Reg. No./Substance:
0/MIRN34 microRNA, human; 0/Membrane Proteins; 0/MicroRNAs; 0/Nerve Tissue Proteins; 0/PRIMA1 protein, human; 0/RNA, Messenger; 0/Tumor Suppressor Protein p53

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