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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
MiR-1306-5p promotes cell proliferation and inhibits cell apoptosis in acute myeloid leukemia by downregulating PHF6
Xiang Gao1, Sumei Fan2, Xiaolei Zhang3
1Department of Basic Medical Sciences, Medical College, Qinghai University, Xining 810001, Qinghai, China.
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.
Insights
MicroRNA miR-1306-5p acts as an oncogene in acute myeloid leukemia (AML) by promoting cancer cell proliferation and inhibiting apoptosis. This microRNA targets PHF6, suggesting a potential therapeutic target for AML treatment.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Aberrant microRNA (miRNA) expression is implicated in acute myeloid leukemia (AML) pathogenesis.
- This study investigates the specific role and underlying mechanisms of miR-1306-5p in AML development.
Purpose of the Study:
- To elucidate the function of miR-1306-5p in AML.
- To identify the molecular targets and pathways regulated by miR-1306-5p in AML.
Main Methods:
- Expression analysis of miR-1306-5p and PHF6 in AML patient samples and cell lines.
- Functional assays (CCK-8, EdU, TUNEL, flow cytometry) to assess proliferation and apoptosis.
- Bioinformatic prediction (Starbase, miRWalk) and experimental validation of miRNA-target interactions.
Main Results:
- miR-1306-5p is frequently upregulated in AML patient cells and cell lines.
- Downregulation of miR-1306-5p inhibits AML cell proliferation and induces apoptosis.
- miR-1306-5p directly targets PHF6, a transcriptional regulator, which is downregulated in AML.
- PHF6 depletion exacerbates AML cell proliferation and reduces apoptosis.
Conclusions:
- miR-1306-5p promotes AML progression by upregulating PHF6 expression.
- miR-1306-5p functions as an oncogene in AML.
- miR-1306-5p represents a potential therapeutic target for AML treatment.
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