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Updated: Apr 15, 2026

The Soft Agar Colony Formation Assay
Published on: October 27, 2014
Decreased expression of RPS15A suppresses proliferation of lung cancer cells
Xinmin Zhao1,2, Lei Shen2,3, Yu Feng1,2
1Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Abstract:
Lung cancer is the leading cause of cancer-related death in the world. Previous report has identified ribosomal protein s15a (RPS15A) as a TGF-β-responsible gene in the lung adenocarcinoma cell line A549. In this study, we used specific si-RNA to downregulate RPS15A expression in A549 cells and found that decreased RPS15A expression significantly inhibited cell proliferation and survival, as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assays. Moreover, A549 cells were obviously accumulated in the G0/G1 phase in response to RPS15A knockdown, suggesting that RPS15A inhibition could induce a diminution of proliferation through cell cycle arrest. In addition, immunohistochemistry analysis further revealed that RPS15A was overexpressed in surgically resected lung cancer tissues. In conclusion, we identify RPS15A as a novel potential oncogenic gene involved in lung carcinogenesis. This study may provide a preliminary experimental basis for a gene therapy approach for treating lung cancer.
Insights
Ribosomal protein S15a (RPS15A) plays a key role in lung cancer development. Downregulating RPS15A inhibits lung adenocarcinoma cell proliferation and survival, suggesting its potential as a gene therapy target.
Area of Science:
- Oncology
- Molecular Biology
- Gene Expression
Background:
- Lung cancer is a leading cause of cancer-related mortality worldwide.
- Ribosomal protein S15a (RPS15A) was previously identified as a TGF-β-responsive gene in A549 lung adenocarcinoma cells.
Purpose of the Study:
- To investigate the role of RPS15A in lung adenocarcinoma proliferation and survival.
- To evaluate RPS15A as a potential therapeutic target for lung cancer.
Main Methods:
- Specific small interfering RNA (si-RNA) was used to downregulate RPS15A expression in A549 cells.
- Cell proliferation and survival were assessed using MTT and colony formation assays.
- Cell cycle analysis was performed to determine the effect of RPS15A knockdown on cell cycle progression.
- Immunohistochemistry was used to examine RPS15A expression in human lung cancer tissues.
Main Results:
- Decreased RPS15A expression significantly inhibited A549 cell proliferation and survival.
- RPS15A knockdown led to cell cycle arrest at the G0/G1 phase.
- RPS15A was found to be overexpressed in surgically resected lung cancer tissues.
Conclusions:
- RPS15A is identified as a novel oncogenic gene involved in lung carcinogenesis.
- RPS15A inhibition demonstrates potential for lung cancer gene therapy.
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