The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior

Yan Liu; Shannon E. Elf; Takashi Asai; Yasuhiko Miyata; Yuhui Liu; Goro Sashida; Gang Huang; Silvana Di Giandomenico; Andrew Koff; Stephen D. Nimer

doi:10.4161/cc.8.19.9627

The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior

Yan Liu, Shannon E. Elf, Takashi Asai, Yasuhiko Miyata, Yuhui Liu, Goro Sashida, Gang Huang, Silvana Di Giandomenico, Andrew Koff, Stephen D. Nimer

Research output: Contribution to journal › Review article › peer-review

53 Scopus citations

Abstract

In response to diverse stresses, the tumor suppressor p53 differentially regulates its target genes, variably inducing cell cycle arrest, apoptosis or senescence. Emerging evidence indicates that p53 plays an important role in regulating hematopoietic stem cell (HSC) quiescence, self-renewal, apoptosis and aging. The p53 pathway is activated by DNA damage, defects in ribosome biogenesis, oxidative stress and oncogene induced p19ARF upregulation. We present an overview of the current state of knowledge about p53 (and its target genes) in regulating HSC behavior, with the hope that understanding the molecular mechanisms that control p53 activity in HSCs and how p53 mutations affect its role in these events may facilitate the development of therapeutic strategies for eliminating leukemia (and cancer) propagating cells.

Original language	English (US)
Pages (from-to)	3120-3124
Number of pages	5
Journal	Cell Cycle
Volume	8
Issue number	19
DOIs	https://doi.org/10.4161/cc.8.19.9627
State	Published - Oct 1 2009
Externally published	Yes

Funding

This work was funded by NIH RO1 grant (DK52208 to S.D.N.) and an LLS SCOR grant (S.D.N.). The authors would like to thank John Petrini, Andrew Koff and members of Nimer lab for helpful comments. We also would like to thank Ms. Erica Chuang for help in the preparation of this manuscript.

Keywords

Aging
Apoptosis
Gfi-1
Hematopoietic stem cell
Leukemia stem cell
Necdin
Quiescence
Self-renewal
Slug
p21
p53

ASJC Scopus subject areas

Molecular Biology
Cell Biology
Developmental Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.4161/cc.8.19.9627

Cite this

@article{cfd36b4ec3d245b19e22ef5999961e7d,

title = "The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior",

abstract = "In response to diverse stresses, the tumor suppressor p53 differentially regulates its target genes, variably inducing cell cycle arrest, apoptosis or senescence. Emerging evidence indicates that p53 plays an important role in regulating hematopoietic stem cell (HSC) quiescence, self-renewal, apoptosis and aging. The p53 pathway is activated by DNA damage, defects in ribosome biogenesis, oxidative stress and oncogene induced p19ARF upregulation. We present an overview of the current state of knowledge about p53 (and its target genes) in regulating HSC behavior, with the hope that understanding the molecular mechanisms that control p53 activity in HSCs and how p53 mutations affect its role in these events may facilitate the development of therapeutic strategies for eliminating leukemia (and cancer) propagating cells.",

keywords = "Aging, Apoptosis, Gfi-1, Hematopoietic stem cell, Leukemia stem cell, Necdin, Quiescence, Self-renewal, Slug, p21, p53",

author = "Yan Liu and Elf, {Shannon E.} and Takashi Asai and Yasuhiko Miyata and Yuhui Liu and Goro Sashida and Gang Huang and {Di Giandomenico}, Silvana and Andrew Koff and Nimer, {Stephen D.}",

note = "Funding Information: This work was funded by NIH RO1 grant (DK52208 to S.D.N.) and an LLS SCOR grant (S.D.N.). The authors would like to thank John Petrini, Andrew Koff and members of Nimer lab for helpful comments. We also would like to thank Ms. Erica Chuang for help in the preparation of this manuscript.",

year = "2009",

month = oct,

day = "1",

doi = "10.4161/cc.8.19.9627",

language = "English (US)",

volume = "8",

pages = "3120--3124",

journal = "Cell Cycle",

issn = "1538-4101",

publisher = "Landes Bioscience",

number = "19",

}

TY - JOUR

T1 - The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior

AU - Liu, Yan

AU - Elf, Shannon E.

AU - Asai, Takashi

AU - Miyata, Yasuhiko

AU - Liu, Yuhui

AU - Sashida, Goro

AU - Huang, Gang

AU - Di Giandomenico, Silvana

AU - Koff, Andrew

AU - Nimer, Stephen D.

N1 - Funding Information: This work was funded by NIH RO1 grant (DK52208 to S.D.N.) and an LLS SCOR grant (S.D.N.). The authors would like to thank John Petrini, Andrew Koff and members of Nimer lab for helpful comments. We also would like to thank Ms. Erica Chuang for help in the preparation of this manuscript.

PY - 2009/10/1

Y1 - 2009/10/1

N2 - In response to diverse stresses, the tumor suppressor p53 differentially regulates its target genes, variably inducing cell cycle arrest, apoptosis or senescence. Emerging evidence indicates that p53 plays an important role in regulating hematopoietic stem cell (HSC) quiescence, self-renewal, apoptosis and aging. The p53 pathway is activated by DNA damage, defects in ribosome biogenesis, oxidative stress and oncogene induced p19ARF upregulation. We present an overview of the current state of knowledge about p53 (and its target genes) in regulating HSC behavior, with the hope that understanding the molecular mechanisms that control p53 activity in HSCs and how p53 mutations affect its role in these events may facilitate the development of therapeutic strategies for eliminating leukemia (and cancer) propagating cells.

AB - In response to diverse stresses, the tumor suppressor p53 differentially regulates its target genes, variably inducing cell cycle arrest, apoptosis or senescence. Emerging evidence indicates that p53 plays an important role in regulating hematopoietic stem cell (HSC) quiescence, self-renewal, apoptosis and aging. The p53 pathway is activated by DNA damage, defects in ribosome biogenesis, oxidative stress and oncogene induced p19ARF upregulation. We present an overview of the current state of knowledge about p53 (and its target genes) in regulating HSC behavior, with the hope that understanding the molecular mechanisms that control p53 activity in HSCs and how p53 mutations affect its role in these events may facilitate the development of therapeutic strategies for eliminating leukemia (and cancer) propagating cells.

KW - Aging

KW - Apoptosis

KW - Gfi-1

KW - Hematopoietic stem cell

KW - Leukemia stem cell

KW - Necdin

KW - Quiescence

KW - Self-renewal

KW - Slug

KW - p21

KW - p53

UR - http://www.scopus.com/inward/record.url?scp=70349897697&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70349897697&partnerID=8YFLogxK

U2 - 10.4161/cc.8.19.9627

DO - 10.4161/cc.8.19.9627

M3 - Review article

C2 - 19755852

AN - SCOPUS:70349897697

SN - 1538-4101

VL - 8

SP - 3120

EP - 3124

JO - Cell Cycle

JF - Cell Cycle

IS - 19

ER -

The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this