MiR-221/222 promotes S-Phase entry and cellular migration in control of basal-like breast cancer

Yuan Li, Chunli Liang, Haizhong Ma, Qian Zhao, Ying Lu, Zhendong Xiang, Li Li, Jie Qin, Yihan Chen, William C. Cho, Richard G. Pestell, Li Liang, Zuoren Yu

Research output: Contribution to journalArticlepeer-review

69 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)7122-7137
Number of pages16
JournalMolecules
Volume19
Issue number6
DOIs
Publication statusPublished - Jun 2014
Externally publishedYes

Fingerprint

Dive into the research topics of 'MiR-221/222 promotes S-Phase entry and cellular migration in control of basal-like breast cancer'. Together they form a unique fingerprint.

Cite this