Protein kinase C isoforms and cell proliferation in neuroblastoma cells

被引:9
作者
Cabedo, H [1 ]
Minana, MD [1 ]
Grau, E [1 ]
Felipo, V [1 ]
Grisolia, S [1 ]
机构
[1] FDN VALENCIANA INVEST BIOMED,INST INVEST CITOL,E-46100 VALENCIA,SPAIN
来源
MOLECULAR BRAIN RESEARCH | 1996年 / 37卷 / 1-2期
关键词
protein kinase C; isoforms; cell proliferation; calphostin C; H7; neuroblastoma;
D O I
10.1016/0169-328X(95)00290-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The expression of protein kinase C isoforms in the neuroblastoma cell line Neuro 2a has been studied. It is shown that Neuro 2a cells express alpha, delta, epsilon and zeta PKCs. Inhibition of cell proliferation by using protein kinase C inhibitors (H7 or calphostin C) or medium without glutamine affects markedly the pattern of PKC isoforms. All treatments reduced significantly (50-70%) the content of PKC alpha. None of the treatments altered PKC zeta or epsilon. The content of PKC delta was increased (88-120%) in cells treated with PKC inhibitors but was slightly reduced in cells incubated in medium without glutamine. However, none of the treatments affected the content of the corresponding mRNAs. Long-term treatment of synchronized cells with the phorbol ester PMA depletes PKC alpha but not PKC delta or zeta and only partially PKC epsilon. This treatment with PMA did not affect DNA synthesis, indicating that PKC alpha does not play a significant role in the control of proliferation of these cells.
引用
收藏
页码:125 / 133
页数:9
相关论文
共 24 条
[1]  
BECKER D, 1990, ONCOGENE, V5, P1133
[2]  
Bell R M, 1986, Methods Enzymol, V124, P353
[3]  
BENZIL DL, 1992, CANCER RES, V52, P2951
[4]   PROTEIN KINASE-C-ZETA ISOFORM IS CRITICAL FOR MITOGENIC SIGNAL-TRANSDUCTION [J].
BERRA, E ;
DIAZMECO, MT ;
DOMINGUEZ, I ;
MUNICIO, MM ;
SANZ, L ;
LOZANO, J ;
CHAPKIN, RS ;
MOSCAT, J .
CELL, 1993, 74 (03) :555-563
[5]  
DUNN JA, 1992, CANCER RES, V52, P990
[6]  
FELIPO V, 1990, J BIOL CHEM, V265, P9599
[7]   INDUCTION OF RAT-BRAIN TUBULIN FOLLOWING AMMONIUM INGESTION [J].
FELIPO, V ;
MINANA, MD ;
AZORIN, I ;
GRISOLIA, S .
JOURNAL OF NEUROCHEMISTRY, 1988, 51 (04) :1041-1045
[8]  
FELIPO V, 1994, EUR J CANCER, V30, P524
[9]  
HATADA T, 1992, CANCER, V70, P2918, DOI 10.1002/1097-0142(19921215)70:12<2918::AID-CNCR2820701231>3.0.CO
[10]  
2-5