PMID- 12241115
OWN - NLM
STAT- MEDLINE
DCOM- 20030403
LR  - 20190910
IS  - 0167-594X (Print)
IS  - 0167-594X (Linking)
VI  - 59
IP  - 3
DP  - 2002 Sep
TI  - Growth control of C6 glioma in vivo by nerve growth factor.
PG  - 199-205
AB  - Treatment with nerve growth factor (NGF) causes differentiation of rat C6 glioma 
      cells and strongly inhibits their proliferation in vitro. This suggests that 
      induction of NGF-mediated differentiation may provide a novel therapeutic 
      approach to growth control of glial tumors. We examined the effects of NGF 
      treatment on the growth potential of C6 glioma, which expressed NGF receptor in 
      vivo. C6 glioma cells (1 x 10(6) cells/10 microl) were transplanted into the rat 
      striatum. After 4 days, the animals were given successive injections of 100 ng 
      NGF into the growing tumor at every 4 days (n = 10 rats). Controls were subjected 
      to identical procedures with vehicle which did not contain NGF (n = 10 rats). At 
      14 days after transplantation, we evaluated the tumor volume, proliferative cell 
      index (PCI) based on the MIB-1 immunoreactivity and enzyme activities related to 
      energy metabolism by enzyme histochemistry. We found that the NGF treatment 
      markedly reduced the tumor volume of the C6 glioma (34.00 +/- 8.47 mm3 to 7.22 
      +/- 4.92 mm3, p < 0.01). NGF treatment also decreased the PCI (33.34 +/- 9.57% to 
      3.85 +/- 3.56%, p < 0.01) with a negative correlation with tumor volume (r = 
      0.972, p < 0.01), and the hexokinase (HK) and glucose-6-phosphate dehydrogenase 
      (G6PDH) activities (p < 0.01 and p < 0.01, respectively) which reflect the demand 
      for nucleic acid synthesis for proliferation through the glycolytic and pentose 
      phosphate pathways. The present results demonstrate for the first time that 
      inhibition of tumor cell proliferation of C6 glioma by NGF occurs in vivo, 
      probably through the NGF-mediated differentiation of C6 glioma cells which has 
      been observed in in vitro studies.
FAU - Kimura, Shigeyoshi
AU  - Kimura S
AD  - Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, 
      Japan.
FAU - Yoshino, Atsuo
AU  - Yoshino A
FAU - Katayama, Yoichi
AU  - Katayama Y
FAU - Watanabe, Takao
AU  - Watanabe T
FAU - Fukushima, Takao
AU  - Fukushima T
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Neurooncol
JT  - Journal of neuro-oncology
JID - 8309335
RN  - 0 (Ki-67 Antigen)
RN  - 0 (Nerve Growth Factors)
RN  - EC 1.1.1.49 (Glucosephosphate Dehydrogenase)
RN  - EC 2.7.1.1 (Hexokinase)
SB  - IM
MH  - Animals
MH  - Brain Neoplasms/drug therapy/metabolism/*pathology
MH  - Cell Differentiation
MH  - Cell Division/drug effects
MH  - Glioma/drug therapy/metabolism/*pathology
MH  - Glucosephosphate Dehydrogenase/metabolism
MH  - Hexokinase/metabolism
MH  - Immunoenzyme Techniques
MH  - Ki-67 Antigen/metabolism
MH  - Male
MH  - Neoplasm Transplantation
MH  - Nerve Growth Factors/*pharmacology
MH  - Pentose Phosphate Pathway
MH  - Rats
MH  - Rats, Wistar
MH  - Tumor Cells, Cultured/drug effects
EDAT- 2002/09/21 10:00
MHDA- 2003/04/04 05:00
CRDT- 2002/09/21 10:00
PHST- 2002/09/21 10:00 [pubmed]
PHST- 2003/04/04 05:00 [medline]
PHST- 2002/09/21 10:00 [entrez]
AID - 10.1023/a:1019919019497 [doi]
PST - ppublish
SO  - J Neurooncol. 2002 Sep;59(3):199-205. doi: 10.1023/a:1019919019497.