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PLoS One. 2014 Mar 17;9(3):e91557. doi: 10.1371/journal.pone.0091557. eCollection 2014.

Effects of THAP11 on erythroid differentiation and megakaryocytic differentiation of K562 cells.

Author information

1
Department of Pharmaceutical Engineering, Tianjin University, Tianjin, China; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China.
2
Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China; State Key Laboratory of Proteomics, Beijing, China.
3
Department of Hematopoietic Stem Cell Transplantation, Affiliated Hospital to Academy of Military Medical Sciences, Beijing, China.
4
Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China.
5
Department of Pharmaceutical Engineering, Tianjin University, Tianjin, China.
6
Department of Chemistry, Purdue University, West Lafayette, Indiana, United States of America.
7
Department of Pulmonary Neoplasms Internal Medicine, Affiliated Hospital to Academy of Military Medicine Sciences, Beijing, China.
8
Department of Pharmaceutical Engineering, Tianjin University, Tianjin, China; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China; State Key Laboratory of Proteomics, Beijing, China.

Abstract

Hematopoiesis is a complex process regulated by sets of transcription factors in a stage-specific and context-dependent manner. THAP11 is a transcription factor involved in cell growth, ES cell pluripotency, and embryogenesis. Here we showed that THAP11 was down-regulated during erythroid differentiation but up-regulated during megakaryocytic differentiation of cord blood CD34+ cells. Overexpression of THAP11 in K562 cells inhibited the erythroid differentiation induced by hemin with decreased numbers of benzidine-positive cells and decreased mRNA levels of α-globin (HBA) and glycophorin A (GPA), and knockdown of THAP11 enhanced the erythroid differentiation. Conversely, THAP11 overexpression accelerated the megakaryocytic differentiation induced by phorbol myristate acetate (PMA) with increased percentage of CD41+ cells, increased numbers of 4N cells, and elevated CD61 mRNA levels, and THAP11 knockdown attenuated the megakaryocytic differentiation. The expression levels of transcription factors such as c-Myc, c-Myb, GATA-2, and Fli1 were changed by THAP11 overexpression. In this way, our results suggested that THAP11 reversibly regulated erythroid and megakaryocytic differentiation.

PMID:
24637716
PMCID:
PMC3956667
DOI:
10.1371/journal.pone.0091557
[Indexed for MEDLINE]
Free PMC Article
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