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Previously, we reported that  ZNF300  might play a role in leukemogenesis. In this study, we further investigated the function of ZNF300 in K562 cells undergoing differentiation. We found that ZNF300 upregulation in K562 cells coincided with megakaryocytic differentiation induced by phorbol-12-myristate-13-acetate (PMA) or erythrocytic differentiation induced by cytosine arabinoside (Ara-C), respectively. To further test whether ZNF300 upregulation promoted differentiation, we knocked down  ZNF300  and found that  ZNF300  knockdown effectively abolished PMA-induced megakaryocytic differentiation, evidenced by decreased CD61 expression. Furthermore, Ara-C-induced erythrocytic differentiation was also suppressed in  ZNF300  knockdown cells with decreased γ-globin expression and CD235a expression. These observations suggest that ZNF300 may be a critical factor controlling distinct aspects of K562 cells. Indeed,  ZNF300  knockdown led to increased cell proliferation. Consistently,  ZNF300  knockdown cells exhibited an increased percentage of cells at S phase accompanied by decreased percentage of cells at G0/G1 and G2/M phase. Increased cell proliferation was further supported by the increased expression of cell proliferation marker PCNA and the decreased expression of cell cycle regulator p15 and p27. In addition, MAPK/ERK signaling was significantly suppressed by  ZNF300  knockdown. These findings suggest a potential mechanism by which  ZNF300  knockdown may impair megakaryocytic and erythrocytic differentiation.

ZNF300 Knockdown Inhibits Forced Megakaryocytic Differentiation by Phorbol and Erythrocytic Differentiation by Arabinofuranosyl Cytidine in K562 Cells