Wnt signaling in stem cells and non-small-cell lung cancer.
Evidence suggests that stem cells may be the source of mutant cells that cause cancers to develop and proliferate. Wnt signaling has been shown to promote self-renewal in gut epithelial and hematopoietic stem cells and to trigger critical pathways in carcinogenesis. In this review, we highlight the progress in understanding how the Wnt pathway contributes to stem cell maintenance and its role in lung carcinogenesis. Although the function of stem cells in solid tumor development is unclear, the Wnt pathway's role in determining the fate and self-renewal potential of cancer stem cells suggests a critical role in carcinogenesis and that developing drugs to inhibit this pathway may be of therapeutic interest.
He
Biao
B
Thoracic Oncology Laboratory, Department of Surgery, Comprehensive Cancer Center, University of California-San Francisco, 1600 Divisadero Street, San Francisco, CA 94143, USA.
Barg
Richard N
RN
You
Liang
L
Xu
Zhigong
Z
Reguart
Noemi
N
Mikami
Iwao
I
Batra
Sonny
S
Rosell
Rafael
R
Jablons
David M
DM
D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy / Q000503:physiopathology*; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000503:physiopathology*; D015398:Signal Transduction; D013234:Stem Cells / Q000502:physiology*; D051153:Wnt Proteins / Q000502:physiology*
D051153:Wnt Proteins