MiR-1306-5p promotes cell proliferation and inhibits cell apoptosis in acute myeloid leukemia by downregulating PHF6 expression.

BACKGROUND

Deregulated expression of miRNAs contributes to the development of numerous malignancies, including acute myeloid leukemia (AML). The present work focused on investigating the role of miR-1306-5p in AML pathogenesis and the possible mechanisms.

METHODS

The expression levels of miR-1306-5p and PHF6 were assessed in 30 healthy controls and 48 newly diagnosed AML patients. CCK-8 assay, EdU staining, quantitative real-time PCR, TUNEL assay, western blots, and flow cytometry were used to characterize the changes induced by miR-1306-5p or PHF6 overexpression or inhibition. In addition, Starbase and miRWalk databases were adopted to predict the miR-1306-5p target genes.

RESULTS

Here we reported that upregulation of miR-1306-5p was a frequent event in both primary leukemic cells from AML patients and AML cell lines. Functional assays indicated that downregulation of miR-1306-5p leads to AML cell growth arrest, less proliferation, and elevated rates of apoptosis. Mechanistically, miR-1306-5p targets PHF6, a protein that plays a key role in gene transcription regulation. Our data further showed that PHF6 was downregulated in AML patients and cell lines, and depletion of PHF6 expression using RNA interference further enhanced the proliferation while reducing the apoptosis of those leukemic cells.

CONCLUSION

Our findings show that miR-1306-5p promotes proliferation and prevents apoptosis in AML by directly modulating PHF6 expression and consequently contributes to AML development and progression. miR-1306-5p may function as an oncogene in AML, providing a promising therapeutic target for AML patients.