Abstract
GATA binding protein 1 (GATA‑1) is one of the most important hematopoietic transcription factors in the production of blood cells, such as platelets, eosinophils, mast cells and erythrocytes. GATA‑1 regulates the participation of microRNA (miRNAs/miRs) in erythroid differentiation under normoxia. However, GATA‑1 expression and the regulation of miR‑210‑3p in the context of erythroid differentiation under hypoxia remain unknown. The present study examined the expression levels of GATA‑1 and miR‑210‑3p in the model of erythroid differentiation in K562 cells under hypoxia, and determined the effects of GATA‑1, miR‑210‑3p and SMAD2 on erythroid differentiation through lentivirus transfection experiments. The present study detected increased GATA‑1 expression under hypoxia. Moreover, miR‑210‑3p was identified as a positive regulator of erythroid differentiation, which was upregulated both during erythroid differentiation and in GATA‑1 overexpression experiments under hypoxia. Importantly, in the K562 cell model of erythroid differentiation under hypoxia, miR‑210‑3p was upregulated in a GATA‑1‑dependent manner. Using a double luciferase reporter assay, miR‑210‑3p was identified as a downstream target of GATA‑1‑mediated regulation of erythropoiesis. Gain‑ or loss‑of‑function analysis of miR‑210‑3p identified its importance in erythroid differentiation. Furthermore, it was found that SMAD2 may be a downstream target gene for miR‑210‑3p. Bioinformatics predictions suggested that SMAD2 mediated miR‑210‑3p‑induced regulation of erythroid differentiation. Collectively, the present study provides novel insights into the miRNA regulation of erythroid differentiation.