Abstract
We have previously shown that 14-3-3 protein, a multifunctional adaptor molecule involved in many aspects of signal transduction pathways, is a target antigen for the cancer-associated human monoclonal antibody. Although recent evidences suggest a crucial role of 14-3-3 family members in the control of cell growth and differentiation, their actual contribution toward tumor development is still controversial. In this article, we examined the effect of enforced 14-3-3 overexpression on cell growth of the human lung adenocarcinoma cell line, A549. To address this issue, we obtained 14-3-3 protein-inducible A549 sublines by transfection with 14-3-3 expression vector under the control of dexamethasone-inducible promoter. We found that 14-3-3 protein induction in some of these sublines promoted their cell proliferation. Microscopic observation revealed that morphology of these cells became aggressive multilayer condition, suggesting that malignant phenotypes are also acquired upon ectopic induction of 14-3-3 protein.
Original language | English |
---|---|
Pages (from-to) | 253-257 |
Number of pages | 5 |
Journal | Cytotechnology |
Volume | 33 |
Issue number | 1-3 |
DOIs | |
Publication status | Published - 2000 |
All Science Journal Classification (ASJC) codes
- Biotechnology
- Bioengineering
- Biomedical Engineering
- Clinical Biochemistry
- Cell Biology