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Transforming growth factor beta 1 (TGF beta 1) down-regulates expression and function of proliferation-inducing
M K Shier1, E B Neely, M G Ward
1Department of Microbiology and Immunology, Milton S. Hershey Medical Center, Pennsylvania State University College of Medicine, Hershey 17033, USA.
Abstract:
The epidemiologic association of human papillomavirus (HPV) infection with dysplasia and cervical cancer is well established. Transforming growth factor beta 1 (TGF beta 1) is a growth inhibitory protein for epithelial cells. To examine the phenotype of HPV-transformed cells, we examined expression of TGF beta 1 and a number of cellular proliferation-enhancing molecules which are known to be regulated by TGF beta 1, including bcl-2, c-jun and NFkB. Previous studies had identified significant induction of TGF beta 1 and concomitant down-regulation of other growth stimulatory molecules in experimental papillomas. We used HPV-16 and -18 transformed cell lines. The HPV-16 transformed cells showed down-regulation of bcl-2 and NFkB as well as NFkB function upon TGF beta 1 treatment. The results suggest that TGF beta 1 may exert antiproliferative effects on some HPV-transformed cells by down-regulating expression and function of different proliferation-enhancing molecules. It is uncertain if this function is virus type specific and/or related to state of tumor cell progression.
Insights
Transforming growth factor beta 1 (TGF beta 1) may inhibit human papillomavirus (HPV)-driven cell growth by reducing key proliferation molecules like bcl-2 and NFkB in some HPV-transformed cells.
Area of Science:
- Oncology
- Virology
- Cell Biology
Background:
- Human papillomavirus (HPV) infection is linked to cervical dysplasia and cancer.
- Transforming growth factor beta 1 (TGF beta 1) inhibits epithelial cell growth.
- Previous research indicated TGF beta 1 induction and growth stimulatory molecule downregulation in experimental papillomas.
Purpose of the Study:
- To investigate the phenotype of HPV-transformed cells.
- To examine the expression of TGF beta 1 and its regulation of proliferation-enhancing molecules (bcl-2, c-jun, NFkB).
Main Methods:
- Utilized HPV-16 and HPV-18 transformed cell lines.
- Assessed expression of TGF beta 1, bcl-2, c-jun, and NFkB.
- Evaluated NFkB function following TGF beta 1 treatment.
Main Results:
- HPV-16 transformed cells exhibited TGF beta 1-induced downregulation of bcl-2 and NFkB.
- NFkB function was also reduced in HPV-16 cells upon TGF beta 1 treatment.
Conclusions:
- TGF beta 1 may exert antiproliferative effects on certain HPV-transformed cells.
- This effect is achieved by downregulating key proliferation-enhancing molecules.
- Further research is needed to determine if this is virus type-specific or related to tumor progression stage.