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Published on: March 17, 2020
Tumour growth-suppressive effect of arsenic trioxide in squamous cell lung carcinoma
Leanne Lee Leung1, Sze-Kwan Lam1, Yuan-Yuan Li1
1Division of Respiratory Medicine, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, SAR, P.R. China.
Abstract:
Lung squamous cell carcinoma (SCC) is the second most common subtype of non-small cell lung carcinoma. The anticancer effects of arsenic trioxide (ATO) in lung adenocarcinoma and small-cell lung cancer have previously been reported; however its effects in SCC remain unclear. An MTT assay and western blot analysis were performed to determine cell viability and protein expression, respectively, in the SK-MES-1 and SW900 SCC cell lines following treatment with ATO. Phosphatidylserine externalization, mitochondrial membrane depolarization and cell cycle distribution were studied using flow cytometry and the in vivo effects of ATO on tumour growth were investigated with a xenograft model. The results demonstrated that SK-MES-1 and SW900 SCC cells were sensitive to clinically relevant concentrations of ATO. ATO induced apoptosis, mitochondrial membrane depolarization and G2/M arrest. In addition, treatment with ATO resulted in the downregulation of X-linked inhibitor of apoptosis, B-cell lymphoma-2 (Bcl-2), E2F transcription factor 1 (E2F1), thymidylate synthase and ribonucleotide reductase M1 in addition to the upregulation of Bcl-2 antagonist/killer protein, cleaved poly ADP-ribose polymerase and cleaved caspase 3 in a cell-line specific manner. In the SW900 xenograft model, tumour growth was inhibited by ATO with the formation of apoptotic bodies and downregulation of Bcl-2 and E2F1. In conclusion, ATO suppresses the growth of SCC in vitro and in vivo.
Insights
Arsenic trioxide (ATO) effectively suppresses lung squamous cell carcinoma (SCC) growth by inducing apoptosis and cell cycle arrest. This study clarifies ATO
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Lung squamous cell carcinoma (SCC) is a major subtype of non-small cell lung cancer.
- Anticancer effects of arsenic trioxide (ATO) are known for other lung cancer types, but its role in SCC was unclear.
- Investigating ATO's efficacy in SCC is crucial for potential therapeutic strategies.
Purpose of the Study:
- To evaluate the anticancer effects of arsenic trioxide (ATO) on lung squamous cell carcinoma (SCC) cell lines.
- To elucidate the molecular mechanisms underlying ATO's action in SCC.
- To assess the in vivo efficacy of ATO in a preclinical SCC model.
Main Methods:
- Cell viability was assessed using MTT assays in SK-MES-1 and SW900 SCC cell lines.
- Apoptosis, mitochondrial membrane potential, and cell cycle were analyzed by flow cytometry.
- Protein expression changes were determined via Western blot, and in vivo efficacy was tested using a xenograft model.
Main Results:
- ATO demonstrated sensitivity in SK-MES-1 and SW900 SCC cells at clinically relevant concentrations.
- ATO induced apoptosis, mitochondrial depolarization, and G2/M cell cycle arrest.
- ATO modulated key proteins involved in apoptosis and cell proliferation, and inhibited tumor growth in vivo.
Conclusions:
- Arsenic trioxide exhibits significant in vitro and in vivo anticancer activity against lung squamous cell carcinoma.
- ATO's mechanism involves the induction of apoptosis and cell cycle arrest.
- These findings support further investigation of ATO as a potential treatment for lung SCC.
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