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Review
. 2018 Jan 3:6:1.
doi: 10.1186/s40364-017-0115-6. eCollection 2018.

SALL4 as a transcriptional and epigenetic regulator in normal and leukemic hematopoiesis

Jianchang Yang  1
Affiliations
Review

SALL4 as a transcriptional and epigenetic regulator in normal and leukemic hematopoiesis

Jianchang Yang. Biomark Res. .

Abstract

In recent years, there has been substantial progress in our knowledge of the molecular pathways by which stem cell factor SALL4 regulates the embryonic stem cell (ESC) properties, developmental events, and human cancers. This review summarizes recent advances in the biology of SALL4 with a focus on its regulatory functions in normal and leukemic hematopoiesis. In the normal hematopoietic system, expression of SALL4 is mainly enriched in the bone marrow hematopoietic stem/progenitor cells (HSCs/HPCs), but is rapidly silenced following lineage differentiation. In hematopoietic malignancies, however, SALL4 expression is abnormally re-activated and linked with deteriorated disease status in patients. Further, SALL4 activation participates in the pathogenesis of tumor initiation and disease progression. Thus, a better understanding of SALL4's biologic functions and mechanisms will facilitate development of advanced targeted anti-leukemia approaches in future.

Keywords: Apoptosis; Chromatin modification; Hematopoietic stem and progenitor cells; Mixed-lineage leukemia; Pluripotency; Transgenic; Wnt/β-catenin signaling.

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Conflict of interest statement

Not applicable.Not applicable.The author declares that he has no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
A tentative model for SALL4-regulated epigenetic mechanism in MLL-r leukemia. a Through interacting with MLL fusion oncoprotein, DOT1L, LSD1 and other epigenetic factors, SALL4 may act as a “guide” in modulating the expression levels of specific downstream gene targets. b SALL4-targetd strategies can disrupt MLL fusion oncoprotein function via dysregulated recruitment of essential epigenetic factors
See this image and copyright information in PMC

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