Medical College of Wisconsin
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Nuclear Receptors as Potential Therapeutic Targets for Myeloid Leukemia. Cells 2020 Aug 19;9(9)

Date

08/23/2020

Pubmed ID

32824945

Pubmed Central ID

PMC7563802

DOI

10.3390/cells9091921

Scopus ID

2-s2.0-85089806628 (requires institutional sign-in at Scopus site)   16 Citations

Abstract

The nuclear receptor (NR) superfamily has been studied extensively in many solid tumors and some receptors have been targeted to develop therapies. However, their roles in leukemia are less clear and vary considerably among different types of leukemia. Some NRs participate in mediating the differentiation of myeloid cells, making them attractive therapeutic targets for myeloid leukemia. To date, the success of all-trans retinoic acid (ATRA) in treating acute promyelocytic leukemia (APL) remains a classical and unsurpassable example of cancer differentiation therapy. ATRA targets retinoic acid receptor (RAR) and forces differentiation and/or apoptosis of leukemic cells. In addition, ligands/agonists of vitamin D receptor (VDR) and peroxisome proliferator-activated receptor (PPAR) have also been shown to inhibit proliferation, induce differentiation, and promote apoptosis of leukemic cells. Encouragingly, combining different NR agonists or the addition of NR agonists to chemotherapies have shown some synergistic anti-leukemic effects. This review will summarize recent research findings and discuss the therapeutic potential of selected NRs in acute and chronic myeloid leukemia, focusing on RAR, VDR, PPAR, and retinoid X receptor (RXR). We believe that more mechanistic studies in this field will not only shed new lights on the roles of NRs in leukemia, but also further expand the clinical applications of existing therapeutic agents targeting NRs.

Author List

Pan P, Chen X

Author

Xiao Chen PhD, MD Associate Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Cell Differentiation
Cell Line, Tumor
Humans
Leukemia, Myeloid
Receptors, Cytoplasmic and Nuclear