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Updated: Jun 13, 2026
Protein Transfection of Mouse Lung
Published on: May 15, 2013
Decreased level of PDCD4 (programmed cell death 4) protein activated cell proliferation in the lung of A/J mouse
Soon-Kyung Hwang1, Arash Minai-Tehrani, Hwang-Tae Lim
1Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul, Korea.
Background:
Programmed cell death 4 (PDCD4), a protein that binds to eukaryotic initiation factor 4A (eIF4A), inhibits the initiation of translation. Although a number of tumor suppressors target transcription, Pdcd4 is the first suppressor targeting protein translation, and has also been suggested to function as a tumor suppressor gene in human cancer. The majority of tumor suppressors are mutationally inactivated, but the expression of Pdcd4 is downregulated with progression in a number of human cancer sites, including the lung.
Methods:
An aerosol of lentivirus-shRNA Pdcd4 was delivered into A/J mice, through a nose-only inhalation system twice a week for 1 month.
Results And Conclusions:
Downregulated Pdcd4 resulted in increase levels of antiapoptotic and uPA-regulated proteins. We also found that downregulated Pdcd4 induced the mTOR/p70S6K pathway and cell-cycle proteins. Our results suggest that Pdcd4 may perform a critical function in the regulation of lung cancer cell proliferation.
Insights
Programmed cell death 4 (PDCD4) downregulation increases proteins that promote cancer growth and cell division. This suggests PDCD4 is crucial for regulating lung cancer cell proliferation.
Area of Science:
- Molecular Biology
- Cancer Research
- Translational Control
Background:
- Programmed cell death 4 (PDCD4) inhibits protein translation initiation by binding to eukaryotic initiation factor 4A (eIF4A).
- Unlike many tumor suppressors, PDCD4 targets protein translation, not transcription, and is implicated as a tumor suppressor gene in human cancers.
- PDCD4 expression is downregulated during cancer progression, particularly in lung cancer, contrasting with the mutational inactivation typical of other tumor suppressors.
Purpose of the Study:
- To investigate the functional role of PDCD4 in lung cancer.
- To determine the downstream effects of PDCD4 downregulation on protein expression and cellular pathways.
Main Methods:
- Delivery of lentivirus-shRNA targeting PDCD4 via aerosol inhalation into A/J mice.
- Twice-weekly administration for one month using a nose-only inhalation system.
Main Results:
- Downregulation of PDCD4 led to increased levels of antiapoptotic proteins.
- PDCD4 downregulation elevated levels of urokinase plasminogen activator (uPA)-regulated proteins.
- The study observed induction of the mTOR/p70S6K pathway and cell-cycle proteins following PDCD4 downregulation.
Conclusions:
- PDCD4 plays a critical role in regulating lung cancer cell proliferation.
- The findings suggest PDCD4 acts as a key regulator in the complex pathways governing lung cancer development.
- Understanding PDCD4's function could offer new therapeutic strategies for lung cancer.
