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Effect of 14-3-3 protein induction on cell proliferation of A549 human lung adenocarcinoma
S Kawamoto1, N Iemura, Y Inoue
1Graduate School of Genetic Resources Technology, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan, skawa@ipc.hiroshima-u.ac.jp.
Abstract:
We have previously shown that 14-3-3 protein, amultifunctional adaptor molecule involved in many aspects ofsignal transduction pathways, is a target antigen for thecancer-associated human monoclonal antibody. Although recentevidences suggest a crucial role of 14-3-3 family members inthe control of cell growth and differentiation, their actualcontribution toward tumor development is still controversial. Inthis article, we examined the effect of enforced 14-3-3overexpression on cell growth of the human lung adenocarcinomacell line, A549. To address this issue, we obtained14-3-3 protein-inducible A549 sublines by transfection with14-3-3 expression vector under the control ofdexamethasone-inducible promoter. We found that 14-3-3 proteininduction in some of these sublines promoted their cell proliferation. Microscopic observation revealed that morphologyof these cells became aggressive multilayer condition,suggesting that malignant phenotypes are also acquired uponectopic induction of 14-3-3 protein.
Insights
Overexpressing 14-3-3 protein in lung cancer cells promoted cell proliferation and aggressive phenotypes. This suggests a potential role for 14-3-3 protein in tumor development.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- 14-3-3 proteins are multifunctional adaptor molecules involved in signal transduction.
- Their role in tumor development is controversial, despite involvement in cell growth and differentiation.
- 14-3-3 proteins are target antigens for cancer-associated monoclonal antibodies.
Purpose of the Study:
- To investigate the effect of enforced 14-3-3 protein overexpression on human lung adenocarcinoma cell line A549 growth.
- To determine if 14-3-3 protein contributes to malignant phenotypes.
Main Methods:
- Established dexamethasone-inducible A549 sublines overexpressing 14-3-3 protein via transfection.
- Utilized microscopic observation to assess cell morphology and proliferation.
Main Results:
- Induction of 14-3-3 protein expression promoted cell proliferation in some A549 sublines.
- Overexpression led to aggressive multilayering and acquisition of malignant phenotypes.
Conclusions:
- Enforced 14-3-3 protein overexpression can promote lung adenocarcinoma cell proliferation.
- 14-3-3 protein induction may contribute to the development of malignant phenotypes in lung cancer.
