| Project/Area Number |
05671921
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
SUGAWA Hideo Kyoto Univ., Sch.of Medicine, Laboratory Medicine, lecturer, 医学研究科, 講師 (70162857)
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| Co-Investigator(Kenkyū-buntansha) |
AKAMIZU Takashi Kyoto Univ., Sch.of Medicine, Laboratory Medicine, assistant, 医学研究科, 助手 (20231813)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | thyroid / neoplasm / cell differentiation / tumor supressor gene / Thyroglobulin / 未分化癌 |
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| Research Abstract |
We compared the thyroid differentiation functions of three kinds of heterohybrids : rat thyroid cell (FRTL5)/human undifferentiated thyroid cancer cell (HTC/C3), FRTL5/human fibroblasts (HEL) and FRTL5/human thyrocyte obtained from Graves' patient (Gr) with homohybrids of HTC,FRTL5 and Gr. The HTC-FRTL5 hybrids did not produce thyroid hormone, whereas rat thyroglobulin (rTg) production decreased for the first 6 days, and then increased over the basal level under the presence of TSH.Human Tg (hTg) also became detectable after 6 days concomitantly with recovery of rTg production. Such changes of both Tg productions were not observed in the hybrids cultured in the absence of TSH.When FRTL5 cells were fused with primary cultured Gr or HEL,the production of rTg was not inhibited. Furthermore, de novo production of thyroid hormone was induced in the HEL-FRTL5 hybrid during the first 48 hours, although hTg production was not observed even 10 days after the initial culture of this hybrid cell.
… More
When we introduced full-length wild rat TSH-R gene (T8A) into HTC/C3, they showed significant cAMP production by TSH,but not immunostained hTg production for 10 days. There was no detection of hTg in the media, either. These cells did not show any significant iodide incorporation into the cell. These HTC-T8A cells were further transfected with wild P53 gene. We did not observe apparent apoptotic phenomenone by microscope. The HTC-T8A transfected with P53 did not show positive staining of hTg for 10 days. We also did not detect significant production of hTg in the media. Therefore, we concluded that introduction of TSH-R and wild P53 is insuffcient for the newly induction of hTg and iodide incorporation mechanism in HTC/C3. Our observation suggest the contribution of both mechanisms of absent differentiation factor (s) and present dediferrentiated factor (s) in human undifferentiated cancer cell HTC.The relationship between such putative factors and undifferentiation-tumorgenesis of thyroid must be elucidated in order to better understand the regulation of thyroidal differentiation and neoplastic transformation. Less
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