Aerosol-delivered programmed cell death 4 enhanced apoptosis, controlled cell cycle and suppressed AP-1 activity in the lungs of AP-1 luciferase reporter mice
Abstract
The long-term survival of lung cancer patients treated with conventional therapies remains poor and therefore the need for novel approaches remains high. This has led to the re-emergence of aerosol delivery as a therapeutic intervention. In this study, glucosylated polyethylenimine (GPEI) was used as carrier to investigate programmed cell death 4 (PDCD4) and PDCD4 mutant (D418A), an eIF4A-binding mutant, on PDCD4-related signaling and activator protein-1 (AP-1) activity in the lungs of AP-1 luciferase reporter mice. After confirming the efficiency of GPEI as a carrier in lungs, the effects of aerosol-delivered PDCD4 were investigated in AP-1 luciferase reporter mice. Aerosol delivery of GPEI/PDCD4 through a nose-only inhalation facilitated the apoptosis of lungs whereas aerosol PDCD4 mutant did not. Also, such aerosol delivery regulated proteins relevant to cell-cycle control and suppressed AP-1 activity. Results obtained by western blot analysis, immunohistochemistry, luciferase assay and deoxynucleotidyl-transferase-mediated nick end labeling study suggest that combined actions such as facilitating apoptosis, controlling cell cycle and suppression of AP-1 activity by PDCD4 may provide useful tool for designing lung tumor prevention and treatment by which PDCD4 functions as a transformation suppressor in the future.
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Aerosol delivery of Pdcd4 cDNA into cancerous mouse lung inhibits tumor cell proliferation and induces tumor cell apoptosis.
“Huang et al. delivered Pdcd4 cDNA into cancerous mouse lung by aerosol delivery and observed the inhibition of tumor cell proliferation and induction of tumor cell apoptosis [103].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [103]
Pdcd4 functions both as an inducer of apoptosis and a suppressor of AP-1 activity.
“Pdcd4 functions both as an inducer of apoptosis and a suppressor of AP-1 activity (Hwang et al., 2007).”
From Modulation of K-Ras-Dependent Lung Tumorigenesis by MicroRNA-21 (2010) · cites this paper as Hwang et al., 2007
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- Authors
- Hwang, S.-K., Jin, H., Kwon, J. T., Chang, S.-H., Kim, T. H., Cho, C.-S., Lee, K. H., Young, M. R., Colburn, N. H., Beck, G. R., Yang, H.-S., & Cho, M.-H.
- Affiliations
- Seoul National University (KR)
- Korea Institute of Radiological and Medical Sciences (KR)
- National Cancer Institute (US)
- Emory University (US)
- University of Kentucky (US)
- Corresponding author
- Cho, M-H
- Venue
- Gene Therapy
- Published
- 2007-07-05
- Volume
- 14
- Issue
- 18
- Pages
- 1353-1361
- ISSN
- 0969-7128 (ISSN-L)
- 1476-5462
- OpenAlex
- W2070300401
- Cited by
- 44
- References
- 23
- Citations by year
- 2022: 2 · 2021: 1 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 2 · 2014: 3 · 2013: 3 · 2012: 4
- FWCI
- 1.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Gene Therapy (publishedVersion)
- PubMed (publishedVersion)
- Seoul National University Open Repository (Seoul National University) (submittedVersion)
- Funders
- National Cancer Institute (CA 84573, K22CA084573)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Inhalation and Respiratory Drug Delivery
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- PDCD4, aerosol drug delivery, apoptosis, cell cycle regulation, lung cancer
- MeSH terms
- Aerosols, Animals, Cell Cycle, Immunohistochemistry, Luciferases, Lung, Lung Neoplasms, Mice, Inbred C57BL, Mice, Inbred DBA, Polyethyleneimine, Transfection, Genetic Therapy, Gene Expression, RNA-Binding Proteins, Apoptosis, Transcription Factor AP-1, In Situ Nick-End Labeling, Models, Animal, Apoptosis Regulatory Proteins, Mice
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