| Summary: | 碩士 === 國立成功大學 === 微生物及免役學研究所 === 82 === Malignant glioma is one of the most common tumors affecting
human central nervous system (CNS). Insulin existing in the CNS
can promote the growth of neuron and acts as a neuromodulator.
When grew in insulin-containing medium, the Ser/Thr
phosphorylation was low in gliomas, but was high in normal
glial cells. In gliomas, the descend of phosphorylation
activity by insulin was detected in the ten minutes and reached
to minimum after five hours. The raise of phosphorylation
activity in glial cells by insulin followed a similar reaction
time mode. The regulation of phosphorylation by insulin was
dose-dependent; significant inhibition in gliomas was detected
as low as 500 ng/ml of insulin. IGF-I could notsuppress the
phosphorylation activity in gliomas. The change of
phosphorylation activity induced by insulin could be partly
inhibited by actinomycin D and cycloheximide. The cell growth
rate was more affected by insulin along with the increase of
concentration of fetal calf serum. Glioma cells cultured in
insulin-containing medium grew more faster than those cultured
in insulin-free medium. On the contrary, insulin reduced the
growth rate of glial cells. Insulin treatment did not lead
morphological change of both glioma and glial cells. After
insulin stimulation, the total PKC activities of gliomas were
increased, but that of glial cells were decreased. Using
Western-blotting, the PKC-a, b, d, g, and e subspecies proteins
in glial cells were not detected regardless with or without
insulin stimulation. The PKC-a, b, and d were constitutively
expressed in the cytosolic fraction of gliomas. Insulin would
down-regulate the expression of PKC-e in the membrane fraction
and PKC-g in the cytosolic fraction of gliomas.
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