MicroRNA-9 restrains the sharp increase and boost apoptosis of human acute myeloid leukemia cells by adjusting the Hippo/YAP signaling pathway

ABSTRACT

MicroRNAs (miRNAs) play a very important role in the development of acute myeloid leukemia (AML). This study focuses on the effects of miR-9 on the regulation of AML cells and their related signaling pathways. We found that the expression of miR-9 was significantly decreased in four AML cell lines (THP-1, HL-60, TF-1 and KG-1) compared with the human normal bone marrow cells (HS-5). Moreover, miR-9 overexpression inhibited HL-60 cell proliferation ability, and promoted apoptosis. However, interfering with miR-9 expression promoted the proliferation of HL-6 cells and inhibited apoptosis. Western blotting results subsequently showed that overexpression of miR-9 could elevate the expression of MAT1, LATS1, and LATS2 in HL-60 cells, and inhibit the expression of YAP, while the interference with miR-9 had the opposite result. Taken together, miR-9 may act as a tumor suppressor by activating the Hippo/YAP signaling pathway of AML cells, which in this way supply ideas for the clinical remedy of AML patients.

Graphical abstract

KEYWORDS:

• mir-9
• Hippo/YAP signaling pathway
• acute myeloid leukemia
• proliferation and apoptosis

Highlights

1. The expression of miR-9 is significantly decreased in AML cancer cell lines.

2. miR-9 overexpression inhibits HL-60 cell proliferation and promoted cell apoptosis.

3. miR-9 overexpression activates the Hippo/YAP signaling pathway.

Availability of data and materials

All data, models, and code generated or used during the study appear in the submitted article.

Ethics approval and consent to participate

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Acknowledgements

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Authors’ contribution

Study concept and design: GW; Acquisition of data: XY, JX; Analysis and interpretation of data: JS, HH, YL; Drafting of the manuscript: GW; Critical revision of the manuscript for important intellectual content: GW; Statistical analysis: JS, HH, YL; Administrative, technical, and material support: XY, JX; Study supervision: GW; all authors have read and approved the manuscript

Disclosure statement

No potential conflict of interest was reported by the author(s).

Supplementary material

Supplemental data for this article can be accessed here.

Additional information

Funding

We receive no funding to support the research.