Document Detail

Suppression of proline-directed protein kinase F(A) systemically inhibits the growth of human acute leukemia cells.
MedLine Citation:
PMID:  11267978     Owner:  NLM     Status:  MEDLINE    
Initial studies revealed that proline-directed protein kinase F(A) (PDPK F(A)) was overexpressed in various cancerous tissues relative to normal controls. However, the functional role of overexpressed PDPK F(A) in cancer remains to be established. In this report, we explore the potential role of PDPK F(A) in leukemia cell growth by investigating the effects of partial inhibition of this kinase on human acute promyelocytic leukemia (HL-60) and acute lymphoblastic leukemia (Jurkat) cells. Cloning of PDPK F(A) cDNA and its recombinant antisense expression vector and antibody were successfully developed. Several stable antisense clones of HL-60 and Jurkat cells were subcloned, which expressed a low level of PDPK F(A) when compared with the control-transfected clone in immunoblot analysis. Moreover, these antisense clones potently inhibited cell growth, clonogenic growth in soft agar and serum-independent growth. The results taken together demonstrate that suppression of PDPK F(A) is able to interfere with the growth of HL-60 and Jurkat cells, suggesting an essential role of this PDPK in human acute leukemia cell growth.
C P Hsu; C C Yang; S D Yang
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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:  91     ISSN:  0020-7136     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2001 Mar 
Date Detail:
Created Date:  2001-03-27     Completed Date:  2001-04-19     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  650-53     Citation Subset:  IM    
Copyright Information:
Copyright 2001 Wiley-Liss, Inc.
Department of Life Science, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
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MeSH Terms
Cell Division
Cloning, Molecular
DNA, Complementary / metabolism
HL-60 Cells
Jurkat Cells
Leukemia, Promyelocytic, Acute / drug therapy*,  enzymology*
Oligonucleotides, Antisense / metabolism
Proline-Directed Protein Kinases
Protein-Serine-Threonine Kinases / metabolism*
Recombinant Proteins / metabolism
Time Factors
Reg. No./Substance:
0/DNA, Complementary; 0/Oligonucleotides, Antisense; 0/Recombinant Proteins; EC 2.7.11.-/Proline-Directed Protein Kinases; EC Kinases

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