1995 Fiscal Year Final Research Report Summary
Changes in gene activity of growth factors and their receptorsand the contentsof growth factors in urine during bladder carcinogenesis.
| Project/Area Number |
06671595
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Urology
|
|---|
| Research Institution | Kagawa Medical School |
|---|
Principal Investigator |
NISHI Nozomu Kagawa Medical School, Dept.of Endocrinology, Research Associate, 医学部, 助手 (10145047)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MATSUOKA Noriyoshi Kagawa Medical School, Dept of Urology, Assistant Professor, 医学部・附属病院, 講師 (20165781)
|
|---|
| Project Period (FY) |
1994 – 1995
|
| Keywords | Bladder carcinoma / Growth factors / Growth factor receptors / Metastasis / Cell motility / HGF / c-met / TGF-alpha |
|---|
| Research Abstract |
To investigate the roles of growth factors in bladder cancer, changes in expression of mRNAs for several growth factors and their receptors were examined during rat bladder carcinogenesis induced with N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) and in clinical specimens. Northern blot analysis showed that the contents of mRNAs for transforming growth factor-alpha (TGF-alpha) and c-met/hepatocyte growth factor (HGF) receptor increased on BBN treatment, Epidermal growth factor (EGF) receptor mRNA was slightly increased with the treatment. While those for fibroblast growth factor (FGF) receptor 1 and transforming growth factor beta (TGF-beta) type II receptor decreased on BBN treatment. The contents of mRNAs for the other factors investigated (EGF,bFGF,KGF,HGF,TGF-beta1) were hardly affected with the treatment or below detectable level. In case of human bladder specimens, the content of c-met mRNA but not TGF-alpha mRNA was high in all the tumor tissues (6 specimens) examined. A rat bladder tumor cell line, NBT-II,expressed both TGF-alpha and c-met mRNAs, and HGF showed apparent scattering and growth stimulating effects on the cells. Human bladder tumor cell lines (UM-UC-3 and T-24) were also susceptible to the cell scattering action of HGF.
These results indicate the possibilities that TGF-alpha produced by a bladder cancer in addition to urinary EGF play a role in the development of rat bladder cancer, and that enhanced cell motility due to activation of the c-met/HGF receptor participates in the invasion and metastasis of both rat and human bladder cancer cells.
|
