Effects of TGF-beta onthe HPC-16-induced Neoplastic Transformation of Human Cells.
- Author:
Il Soo PARK
;
Yoon Soon LEE
;
Chun Hee LEE
;
Sam Sik KIM
;
Dae Han KIM
;
Kwang Soo KIM
;
Jae Ho YANG
- Publication Type:Original Article
- Keywords:
HPV-16;
TGF-b;
Human cell
- MeSH:
Blotting, Northern;
Clone Cells;
Contact Inhibition;
Epithelial Cells;
Fibronectins;
Human papillomavirus 16;
Humans*;
Plasmids;
Receptors, Transforming Growth Factor beta;
RNA;
Transforming Growth Factor beta*;
Transforming Growth Factor beta1
- From:Korean Journal of Gynecologic Oncology and Colposcopy
1997;8(3):243-249
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Human epithelial cell line immortalized with Ad12-SV40 hybrid virus was transfected with plasmid containing HPV-16 gene. Among these clones, clone-3 and clone-6 showed neoplastic transformation properties of contact inhibition, anchorage independence and cellular adhesion after 7 subcultures. The results suggest that SV40 gene in the immortalized human cell system be in concert with HPV-16 in the process of neoplastic transformation of human cells. While TGF-Beta1(5ng/ml) inhibited growth of contml cells and clone-1 cells which did not show transformation, there was no significant change on the growth of clone-3 cells with transformation properties. When transcriptional level of fibronectin on control cells and clone-3 cells were analyzed with northern blot technique, transcription of fibronectin an clone-3 cells were higher, as compared with control cells. RNA hybridization techniques were performed to compare trasnscriptional levels of TGF-Beta1 between control cells and clone-3 cells. RNA level on clone-3 cells with transformation properties was higher than on control cells. These studies indicate that TGF-Beta1 is associated with increases of fibronectin, which may lend to changes of TGF-Beta receptor and loss of its inhibitory action on the transformed cells. Thus, it seems that loss of inhibitory action of TGF-Beta which is mediated by changes of fibronectin may account for a possible mechanism of action in the HPV-16 induced transformation of human cells.
