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Cited by 1,400

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

The microRNA miR-34a inhibits prostate cancer stem cells and metastasis by directly repressing CD44

Open access
Liu, Can, Kelnar, Kevin, Liu, Bigang, Chen, Xin, Calhoun-Davis, Tammy, Li, Hangwen, Patrawala, Lubna, Yan, Hong, Jeter, Collene, Honorio, Sofia, Wiggins, Jason F, Bader, Andreas G, Fagin, Randy, Brown, David, Tang, Dean G·2011·Nature Medicine
DOI 10.1038/nm.2284
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Abstract

Cancer stem cells (CSCs), or tumor-initiating cells, are involved in tumor progression and metastasis. MicroRNAs (miRNAs) regulate both normal stem cells and CSCs, and dysregulation of miRNAs has been implicated in tumorigenesis. CSCs in many tumors—including cancers of the breast, pancreas, head and neck, colon, small intestine, liver, stomach, bladder and ovary—have been identified using the adhesion molecule CD44, either individually or in combination with other marker(s). Prostate CSCs with enhanced clonogenic and tumor-initiating and metastatic capacities are enriched in the CD44+ cell population, but whether miRNAs regulate CD44+ prostate cancer cells and prostate cancer metastasis remains unclear. Here we show, through expression analysis, that miR-34a, a p53 target, was underexpressed in CD44+ prostate cancer cells purified from xenograft and primary tumors. Enforced expression of miR-34a in bulk or purified CD44+ prostate cancer cells inhibited clonogenic expansion, tumor regeneration, and metastasis. In contrast, expression of miR-34a antagomirs in CD44− prostate cancer cells promoted tumor development and metastasis. Systemically delivered miR-34a inhibited prostate cancer metastasis and extended survival of tumor-bearing mice. We identified and validated CD44 as a direct and functional target of miR-34a and found that CD44 knockdown phenocopied miR-34a overexpression in inhibiting prostate cancer regeneration and metastasis. Our study shows that miR-34a is a key negative regulator of CD44+ prostate cancer cells and establishes a strong rationale for developing miR-34a as a novel therapeutic agent against prostate CSCs.

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Metadata

Authors
Liu, C., Kelnar, K., Liu, B., Chen, X., Calhoun-Davis, T., Li, H., Patrawala, L., Yan, H., Jeter, C., Honorio, S., Wiggins, J. F., Bader, A. G., Fagin, R., Brown, D., & Tang, D. G.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2011-01-16
Volume
17
Issue
2
Pages
211-215
ISSN
  • 1078-8956 (ISSN-L)
  • 1546-170X
DOI
10.1038/nm.2284
OpenAlex
W2170685293
Cited by
1,400
References
3
FWCI
46.61
Type
journal article
Language
en
Open access
green

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