miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis (Nat Cell Biol, 2010, 12:247-256)

報告日期: 2010/10/08
報告時間: 16:00/16:50
報告學生: 盧佳杏
講評老師: 呂佩融

Full Text:  http://basicmed.med.ncku.edu.tw/admin/up_img/991008-3.pdf

miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis

Li Ma et al, Nature cell biology 12, 247-256, 2010


Speaker: 盧佳杏 

Commentator: 呂佩融 老師

Date: 10/08/2010

Time: 04:10 p.m.

Room: 602



Cancer metastasis is the overwhelming cause of mortality in patients with solid tumours. Accumulating evidence indicates that epithelial-mesenchymal transition (EMT), a process in which cells undergo a switch from an epithelial phenotype to a mesenchymal phenotype, gives rise to the dissemination of single carcinoma cells from the sites of the primary. And a small-noncoding RNAs named microRNAs are associated with cancer progression and therapeutic outcome in several human cancers. Although the oncogenic or tumor-suppressing functions of several microRNAs have been characterized, the mechanistic roles played by microRNAs directly regulate the EMT is still unclear. In this study, the author found that miR-9, which is over-expressed in breast cancer, directly targets the E-cadherin. Loss of E-cadherin promotes cancer cell metastasis not induce EMT to form micro-metastases in vivo but contribute angiogenesis by activate β-catenin signaling. On the other hand, silencing miR-9 in highly metastatic cells using ‘miRNA sponge’ blocks metastasis. Furthermore, the upregulation of miR-9 is activated by MYC and MYCN that directly bind to miR9-3 locus. In human samples, miR-9 levels significantly correlate with MYCN amplification and metastatic status. In conclusion, the author defines the function of miR-9 and it can be regulated by oncoprotein. These findings illuminate another molecular mechanism for metastasis and microRNAs might as novel clinical biomarkers and therapeutic targets in cancer progression.



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