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Arsenic oxide targets stem cell marker CD133/prominin-1 in gallbladder carcinoma
Zhilong Ai1, Hongtao Pan, Tao Suo
1Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.
Abstract:
CD133+ tumor cells are responsible for the initiation, propagation and recurrence of tumors, which raises the question of how to effectively target CD133+ tumor cells. Arsenic trioxide (As2O3) has considerable efficacy in treating solid tumors with induction of apoptosis. Here, we found that purified CD133+ gallbladder carcinoma cells are highly resistant to conventional chemotherapy. However, As2O3 effectively induces CD133+ gallbladder carcinoma cells apoptosis. Treatment with As2O3 reduces CD133 expression at transcriptional levels. Furthermore, the ectopic expression of CD133 attenuated the apoptotic effect of As2O3 on cells through activation of AKT signaling pathways. Collectively, As2O3 effectively targets CD133 in gallbladder carcinoma, providing a new mechanism of As2O3-induced cell apoptosis and a better understanding of drug resistance in gallbladder carcinoma.
Insights
Arsenic trioxide effectively targets CD133+ gallbladder cancer cells, inducing apoptosis and overcoming chemotherapy resistance. This study reveals a new mechanism for arsenic trioxide
Area of Science:
- Oncology
- Cancer Cell Biology
- Pharmacology
Background:
- CD133+ tumor cells drive tumor initiation, propagation, and recurrence, posing a challenge for effective cancer therapy.
- Arsenic trioxide (As2O3) demonstrates efficacy in solid tumors by inducing apoptosis, but its specific targeting of CD133+ cells requires elucidation.
Purpose of the Study:
- To investigate the efficacy of arsenic trioxide against CD133+ gallbladder carcinoma cells, which exhibit resistance to conventional chemotherapy.
- To elucidate the mechanism by which arsenic trioxide targets CD133+ cells and overcomes drug resistance.
Main Methods:
- Purification of CD133+ gallbladder carcinoma cells.
- Treatment of cells with arsenic trioxide (As2O3).
- Assessment of apoptosis induction and CD133 expression levels.
- Investigation of the role of CD133 ectopic expression and AKT signaling pathways.
Main Results:
- CD133+ gallbladder carcinoma cells showed high resistance to conventional chemotherapy.
- Arsenic trioxide effectively induced apoptosis in CD133+ gallbladder carcinoma cells.
- As2O3 treatment led to a reduction in CD133 expression at the transcriptional level.
- Ectopic expression of CD133 attenuated As2O3's apoptotic effect via AKT pathway activation.
Conclusions:
- Arsenic trioxide is an effective therapeutic agent against CD133+ gallbladder carcinoma.
- As2O3 targets CD133+ cells by reducing CD133 expression and inducing apoptosis, offering a novel mechanism of action.
- This study enhances understanding of drug resistance mechanisms in gallbladder carcinoma and highlights As2O3's potential in overcoming it.
