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miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia
Xuewu Zhang1, Yu Xu1, Jinghan Wang1
1Department of Hematology, Zhejiang University School of Medicine First Affiliated Hospital, Hangzhou, China.
Abstract:
Objective: The study aims to investigate the effects of miR-221-3p in bone marrow mesenchymal stem cell (BMMSC)-derived microvesicles (MVs) on cell cycle, proliferation and invasion of acute myelocytic leukemia (AML). Methods: Bioinformatics was used to predict differentially expressed miRNAs (DEmiRNAs) in AML. The morphology of BMMSC-derived MVs was observed under an electron microscope, and the positional relation of MVs and OCI-AML2 cells was observed by a fluorescence microscope. MTT, Transwell, and flow cytometry assays were used to analyze the effects of MVs on OCI-AML2 cells. The targeted relationship between miR-221-3p and CDKN1C was detected by dual luciferase assay. Results: It was verified that miR-221-3p promoted the proliferation, invasion and migration of OCI-AML2 cells, and induced the cell cycle arrest in G1/S phase as well as inhibited cell apoptosis. Further studies showed that MVs promoted the proliferation, migration and invasion of AML, and induced the cell cycle arrest in G1/S phase through miR-221-3p. It was confirmed that miR-221-3p can directly target CDKN1C to regulate cell cycle, proliferation and invasion of AML. Conclusion: miR-221-3p in BMMSC-derived MVs regulated AML cell cycle, cell proliferation and invasion through targeting CDKN1C. miR-221-3p and CDKN1C were considered to be potential targets and biomarkers for the treatment of AML in clinic.
Insights
Microvesicles from bone marrow mesenchymal stem cells carrying miR-221-3p promote acute myelocytic leukemia (AML) cell proliferation and invasion by targeting CDKN1C. This suggests miR-221-3p and CDKN1C are potential therapeutic targets for AML treatment.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- Acute myelocytic leukemia (AML) remains a significant challenge in hematology.
- Microvesicles (MVs) derived from mesenchymal stem cells are emerging as potential therapeutic agents.
- Understanding the role of specific microRNAs within MVs is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the impact of miR-221-3p within bone marrow mesenchymal stem cell (BMMSC)-derived MVs on AML cell behavior.
- To elucidate the molecular mechanisms underlying the effects of miR-221-3p on AML cell cycle, proliferation, and invasion.
- To identify potential therapeutic targets and biomarkers for AML treatment.
Main Methods:
- Bioinformatic prediction of differentially expressed miRNAs in AML.
- Characterization of BMMSC-derived MVs using electron and fluorescence microscopy.
- Assessment of MV effects on OCI-AML2 cells via MTT, Transwell, and flow cytometry assays.
- Dual luciferase assay to confirm the targeting relationship between miR-221-3p and CDKN1C.
Main Results:
- miR-221-3p was found to enhance OCI-AML2 cell proliferation, invasion, and migration.
- miR-221-3p induced G1/S phase cell cycle arrest and inhibited apoptosis in AML cells.
- BMMSC-derived MVs promoted AML progression through miR-221-3p, which directly targets CDKN1C to regulate cell cycle and proliferation.
Conclusions:
- miR-221-3p within BMMSC-derived MVs plays a critical role in regulating AML cell cycle, proliferation, and invasion by targeting CDKN1C.
- miR-221-3p and CDKN1C represent promising therapeutic targets and biomarkers for clinical application in AML treatment.
