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MicroRNAs contribute to promyelocyte apoptosis in As2O3-treated APL cells
Haihai Liang1, Xuelian Li, Lu Wang
1Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Harbin, P. R. China.
Background:
Arsenic trioxide (As2O3), an ancient drug used in traditional Chinese medicine, has substantial anticancer activities, especially in the treatment of patients suffering from acute promyelocytic leukemia (APL); however the underlying mechanisms are not well understood.
Methods:
MTT assay was used to detect the cell viability. Flow Cytometry analysis and caspase-3 activity assay were used to measure apoptosis of APL cells. Caspase-3 and Bax levels were analyzed by western blot and let-7d and miR-766 levels were determined by real-time RT-PCR.
Results:
As2O3 significantly inhibited cell viability and induced apoptosis in APL cells. Several microRNAs, including let-7d and miR-766, were dysregulated in APL cells treated with As2O3. The expression of caspase-3 and Bax, which are targets of let-7d and miR-766, respectively, were up-regulated in As2O3 treated cells. Transfection of let-7d and miR-766 into NB4 cells decreased the expression of caspase-3 and Bax, respectively. Correspondingly, transfection of these microRNAs increased NB4 cell viability. As2O3 induced degradation of promyelocytic leukemia (PML), and then induced the down-regulation of both let-7d and miR-766 in NB4 cells.
Conclusions:
We construct a dysregulated microRNA network involved in As2O3-induced apoptosis in APL. Targeting this network may be a new strategy for the prevention of side effects associated with APL treatment with As2O3.
Insights
Arsenic trioxide induces apoptosis in acute promyelocytic leukemia (APL) cells by regulating microRNAs (let-7d and miR-766). Targeting this microRNA network may offer new strategies for APL treatment.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Arsenic trioxide (As2O3) exhibits anticancer properties, particularly in acute promyelocytic leukemia (APL).
- The precise mechanisms underlying As2O3's efficacy in APL remain incompletely understood.
Purpose of the Study:
- To elucidate the molecular mechanisms of As2O3-induced apoptosis in APL cells.
- To investigate the role of microRNAs in As2O3's anti-leukemic effects.
Main Methods:
- Cell viability was assessed using MTT assays.
- Apoptosis was measured by flow cytometry and caspase-3 activity assays.
- MicroRNA (let-7d, miR-766), caspase-3, and Bax expression levels were quantified using real-time RT-PCR and western blotting.
Main Results:
- As2O3 significantly reduced APL cell viability and induced apoptosis.
- As2O3 treatment dysregulated let-7d and miR-766 expression, leading to increased caspase-3 and Bax levels.
- Transfection of let-7d and miR-766 suppressed caspase-3 and Bax, respectively, enhancing cell viability.
Conclusions:
- A dysregulated microRNA network (let-7d, miR-766) is implicated in As2O3-induced apoptosis in APL.
- Targeting this microRNA network presents a potential therapeutic strategy to mitigate side effects in APL treatment.
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