Journal
MOLECULES
Volume 19, Issue 6, Pages 7122-7137Publisher
MDPI AG
DOI: 10.3390/molecules19067122
Keywords
miR-221; miR-222; basal-like breast cancer; migration; cell cycle
Funding
- Natural Science Foundation of China [81172515]
- National Basic Research Program of China [2012CB966800]
- Science and Technology Commission of Shanghai Municipality [13JC1401702, 124119a7100]
- Foundation for Innovative Research Groups of the NSFC [81221001]
- NSFC [31000526]
- Kimmel Cancer Center NIH Cancer Center Core grant [P30CA056036]
- Ralph and Marian C. Falk Medical Research Trust
- Pennsylvania Department of Health
- [R01CA70896]
- [R01CA75503]
- [R01CA107382]
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The miR-221/222 cluster has been demonstrated to function as oncomiR in human cancers. miR-221/222 promotes epithelial-to-mesenchymal transition (EMT) and confers tamoxifen resistance in breast cancer. However, the effects and mechanisms by which miR-221/222 regulates breast cancer aggressiveness remain unclear. Here we detected a much higher expression of miR-221/222 in highly invasive basal-like breast cancer (BLBC) cells than that in non-invasive luminal cells. A microRNA dataset from breast cancer patients indicated an elevated expression of miR-221/222 in BLBC subtype. S-phase entry of the cell cycle was associated with the induction of miR-221/222 expression. miRNA inhibitors specially targeting miR-221 or miR-222 both significantly suppressed cellular migration, invasion and G1/S transition of the cell cycle in BLBC cell types. Proteomic analysis demonstrated the down-regulation of two tumor suppressor genes, suppressor of cytokine signaling 1 (SOCS1) and cyclin-dependent kinase inhibit 1B (CDKN1B), by miR-221/222. This is the first report to reveal miR-221/222 regulation of G1/S transition of the cell cycle. These findings demonstrate that miR-221/222 contribute to the aggressiveness in control of BLBC.
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