The Effect of Phorbol Esters on Cell Growth and Epidermal Growth Factor Receptor Modulation in a Human Gastric Carcinoma Cell Line TMK-1

アクセス数 : 1091
ダウンロード数 : 113

今月のアクセス数 : 1
今月のダウンロード数 : 1
File
HiroshimaJMedSci_38_191.pdf 350 KB 種類 : fulltext
Title ( eng )
The Effect of Phorbol Esters on Cell Growth and Epidermal Growth Factor Receptor Modulation in a Human Gastric Carcinoma Cell Line TMK-1
Creator
Ochiai Atsushi
Kameda Takashi
Takanashi Atsushi
Takekura Naoki
Tahara Eiichi
Source Title
Hiroshima Journal of Medical Sciences
Volume 38
Issue 4
Start Page 191
End Page 195
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
Tumor promoting phorbol esters, 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12, 13-dibutyrate (PDBu), significantly enhanced the growth of human gastric cancer cell line TMK-1, whilst activating protein kinase C. The time course of 125I-epidermal growth factor (EGF) binding to TMK-1 cells after TPA treatment showed a decrease in the number of EGF receptors on TMK-1 cells within 3 hr. Autophosphorylation of EGF receptor decreased in accordance with the decrease of EGF binding by TPA treatment. Scatchard plot analysis of TMK-1 cells after TPA treatment showed that high affinity EGF receptor disappeared at 3hr but the number of EGF receptors increased at 24 hr. These findings suggest that tumor promoting phorbol esters stimulate the cell growth through activation of protein kinase C and modification of EGF receptor of human gastric cancer cell line TMK-1.
Keywords
Phorbol ester
Protein kinase C
Gastric cancer cell
EGF receptor
Descriptions
This research was supported in part by Grants-in Aid for Cancer Research from the Ministry of Education, Science and Culture of Japan and from the Ministry of Health and Welfare for a Comprehensive 10-Year Strategy for Cancer Control, Japan.
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 1989-12
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 2637248