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Downregulation of miRNA-200c Links Breast Cancer Stem Cells with Normal Stem Cells
Downregulation of miRNA-200c
Links Breast Cancer Stem Cells
with Normal Stem Cells
Yohei Shimono,1 Maider Zabala,1 Robert W. Cho,1 Neethan Lobo,1 Piero Dalerba,1 Dalong Qian,1 Maximilian Diehn,1
Huiping Liu,1 Sarita P. Panula,1 Eric Chiao,1 Frederick M. Dirbas,2 George Somlo,3 Renee A. Reijo Pera,1 Kaiqin Lao,4
and Michael F. Clarke1,*
1Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 1050 Arastradero Road, Palo Alto, CA 94304, USA
2Department of Surgery, Stanford University, 300 Pasteur Drive, Stanford, CA 94305, USA
3City of Hope Cancer Center, 1500 East Duarte Road, Duarte, CA 91010, USA
4Applied Biosystems, 850 Lincoln Centre Drive, Foster City, CA 94404, USA
*Correspondence: mfclarke@
DOI 10.1016/j.cell.2009.07.011SUMMARY
Human breast tumors contain a breast cancer stem
cell (BCSC) population with properties reminiscent
of normal stem cells. We found 37 microRNAs that
were differentially expressed between human BCSCs
and nontumorigenic cancer cells. Three clusters,
miR-200c-141, miR-200b-200a-429, and miR-183-
96-182 were downregulated in human BCSCs, normal
human and murine mammary stem/progenitor cells,
and embryonal carcinoma cells. Expression of
BMI1, a known regulator of stem cell self-renewal,
was modulated by miR-200c. miR-200c inhibited
the clonal expansion of breast cancer cells and sup-
pressed the growth of embryonal carcinoma cells
in vitro. Most importantly, miR-200c strongly sup-
pressed the ability of normal mammary stem cells to
form mammary ducts and tumor formation driven
by human BCSCs in vivo. The coordinated downregu-
lation of three microRNA clusters and the similar
functional regulation of clonal expansion by miR-
200c provide a molecular link that connects BCSCs
with normal stem cells.
INTRODUCTION
Cancers arise in tissues and organs that contain proliferating
cells that regenerate old and damaged cells. Typically, these
tissues are maintained by stem cells that have the ability to
self-renew, a pr
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