Role of Cripto-1 in stem cell maintenance and malignant progression

Caterina Bianco, Maria Cristina Rangel, Nadia P. Castro, Tadahiro Nagaoka, Kelly Rollman, Monica Gonzales, David S. Salomon

Research output: Contribution to journalShort survey

67 Citations (Scopus)

Abstract

Cripto-1 is critical for early embryonic development and, together with its ligand Nodal, has been found to be associated with the undifferentiated status of mouse and human embryonic stem cells. Like other embryonic genes, Cripto-1 performs important roles in the formation and progression of several types of human tumors, stimulating cell proliferation, migration, epithelial to mesenchymal transition, and tumor angiogenesis. Several studies have demonstrated that cell fate regulation during embryonic development and cell transformation during oncogenesis share common signaling pathways, suggesting that uncontrolled activation of embryonic signaling pathways might drive cell transformation and tumor progression in adult tissues. Here we review our current understanding of how Cripto-1 controls stem cell biology and how it integrates with other major embryonic signaling pathways. Because many cancers are thought to derive from a subpopulation of cancer stem-like cells, which may re-express embryonic genes, Cripto-1 signaling may drive tumor growth through the generation or expansion of tumor initiating cells bearing stem-like characteristics. Therefore, the Cripto-1/Nodal signaling may represent an attractive target for treatment in cancer, leading to the elimination of undifferentiated stem-like tumor initiating cells.

Original languageEnglish
Pages (from-to)532-540
Number of pages9
JournalAmerican Journal of Pathology
Volume177
Issue number2
DOIs
Publication statusPublished - 01-01-2010
Externally publishedYes

Fingerprint

Stem Cells
Maintenance
Neoplastic Stem Cells
Neoplasms
Embryonic Development
Epithelial-Mesenchymal Transition
Genes
Cell Movement
Cell Biology
Carcinogenesis
Cell Proliferation
Ligands
Growth
Therapeutics

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

Cite this

Bianco, C., Rangel, M. C., Castro, N. P., Nagaoka, T., Rollman, K., Gonzales, M., & Salomon, D. S. (2010). Role of Cripto-1 in stem cell maintenance and malignant progression. American Journal of Pathology, 177(2), 532-540. https://doi.org/10.2353/ajpath.2010.100102
Bianco, Caterina ; Rangel, Maria Cristina ; Castro, Nadia P. ; Nagaoka, Tadahiro ; Rollman, Kelly ; Gonzales, Monica ; Salomon, David S. / Role of Cripto-1 in stem cell maintenance and malignant progression. In: American Journal of Pathology. 2010 ; Vol. 177, No. 2. pp. 532-540.
@article{a8280181cf994eb49dc65cda84a81833,
title = "Role of Cripto-1 in stem cell maintenance and malignant progression",
abstract = "Cripto-1 is critical for early embryonic development and, together with its ligand Nodal, has been found to be associated with the undifferentiated status of mouse and human embryonic stem cells. Like other embryonic genes, Cripto-1 performs important roles in the formation and progression of several types of human tumors, stimulating cell proliferation, migration, epithelial to mesenchymal transition, and tumor angiogenesis. Several studies have demonstrated that cell fate regulation during embryonic development and cell transformation during oncogenesis share common signaling pathways, suggesting that uncontrolled activation of embryonic signaling pathways might drive cell transformation and tumor progression in adult tissues. Here we review our current understanding of how Cripto-1 controls stem cell biology and how it integrates with other major embryonic signaling pathways. Because many cancers are thought to derive from a subpopulation of cancer stem-like cells, which may re-express embryonic genes, Cripto-1 signaling may drive tumor growth through the generation or expansion of tumor initiating cells bearing stem-like characteristics. Therefore, the Cripto-1/Nodal signaling may represent an attractive target for treatment in cancer, leading to the elimination of undifferentiated stem-like tumor initiating cells.",
author = "Caterina Bianco and Rangel, {Maria Cristina} and Castro, {Nadia P.} and Tadahiro Nagaoka and Kelly Rollman and Monica Gonzales and Salomon, {David S.}",
year = "2010",
month = "1",
day = "1",
doi = "10.2353/ajpath.2010.100102",
language = "English",
volume = "177",
pages = "532--540",
journal = "American Journal of Pathology",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "2",

}

Bianco, C, Rangel, MC, Castro, NP, Nagaoka, T, Rollman, K, Gonzales, M & Salomon, DS 2010, 'Role of Cripto-1 in stem cell maintenance and malignant progression', American Journal of Pathology, vol. 177, no. 2, pp. 532-540. https://doi.org/10.2353/ajpath.2010.100102

Role of Cripto-1 in stem cell maintenance and malignant progression. / Bianco, Caterina; Rangel, Maria Cristina; Castro, Nadia P.; Nagaoka, Tadahiro; Rollman, Kelly; Gonzales, Monica; Salomon, David S.

In: American Journal of Pathology, Vol. 177, No. 2, 01.01.2010, p. 532-540.

Research output: Contribution to journalShort survey

TY - JOUR

T1 - Role of Cripto-1 in stem cell maintenance and malignant progression

AU - Bianco, Caterina

AU - Rangel, Maria Cristina

AU - Castro, Nadia P.

AU - Nagaoka, Tadahiro

AU - Rollman, Kelly

AU - Gonzales, Monica

AU - Salomon, David S.

PY - 2010/1/1

Y1 - 2010/1/1

N2 - Cripto-1 is critical for early embryonic development and, together with its ligand Nodal, has been found to be associated with the undifferentiated status of mouse and human embryonic stem cells. Like other embryonic genes, Cripto-1 performs important roles in the formation and progression of several types of human tumors, stimulating cell proliferation, migration, epithelial to mesenchymal transition, and tumor angiogenesis. Several studies have demonstrated that cell fate regulation during embryonic development and cell transformation during oncogenesis share common signaling pathways, suggesting that uncontrolled activation of embryonic signaling pathways might drive cell transformation and tumor progression in adult tissues. Here we review our current understanding of how Cripto-1 controls stem cell biology and how it integrates with other major embryonic signaling pathways. Because many cancers are thought to derive from a subpopulation of cancer stem-like cells, which may re-express embryonic genes, Cripto-1 signaling may drive tumor growth through the generation or expansion of tumor initiating cells bearing stem-like characteristics. Therefore, the Cripto-1/Nodal signaling may represent an attractive target for treatment in cancer, leading to the elimination of undifferentiated stem-like tumor initiating cells.

AB - Cripto-1 is critical for early embryonic development and, together with its ligand Nodal, has been found to be associated with the undifferentiated status of mouse and human embryonic stem cells. Like other embryonic genes, Cripto-1 performs important roles in the formation and progression of several types of human tumors, stimulating cell proliferation, migration, epithelial to mesenchymal transition, and tumor angiogenesis. Several studies have demonstrated that cell fate regulation during embryonic development and cell transformation during oncogenesis share common signaling pathways, suggesting that uncontrolled activation of embryonic signaling pathways might drive cell transformation and tumor progression in adult tissues. Here we review our current understanding of how Cripto-1 controls stem cell biology and how it integrates with other major embryonic signaling pathways. Because many cancers are thought to derive from a subpopulation of cancer stem-like cells, which may re-express embryonic genes, Cripto-1 signaling may drive tumor growth through the generation or expansion of tumor initiating cells bearing stem-like characteristics. Therefore, the Cripto-1/Nodal signaling may represent an attractive target for treatment in cancer, leading to the elimination of undifferentiated stem-like tumor initiating cells.

UR - http://www.scopus.com/inward/record.url?scp=77957277604&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957277604&partnerID=8YFLogxK

U2 - 10.2353/ajpath.2010.100102

DO - 10.2353/ajpath.2010.100102

M3 - Short survey

VL - 177

SP - 532

EP - 540

JO - American Journal of Pathology

JF - American Journal of Pathology

SN - 0002-9440

IS - 2

ER -