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Wen-Lung Ma

Wen-Lung Ma

China Medical University Hospital, Taiwan

Title: Sex and microRNA in cancer stem/progenitor cells

Biography

Wen-Lung Ma received Ph.D. degree from University of Rochester in 2009. After 18 months post-doctorate training in Wilmot Cancer Center, University of Rochester Medical Center, he promoted to Assistant Professor in China Medical University in 2011. He published total 20 papers with 5 major in the Gastroenterology fi eld of highest profi le journals during his Ph.D. and post-doc training period. He then demonstrated his independency with three published papers in cancer stem cell/GYN cancer field this year. He also received long term supports for conducting his study of interests since 2010 from National Science Council, Taiwan.

Abstract

Malignant immature ovarian teratomas (IOT) most occur in women of reproductive age. However, what roles estrogenic signaling plays in IOT is unknown. Cancer stem/progenitor cells (CSPCs) is known to be regulated by small non-coding RNA, miR21, which linked to ovarian malignancies. In this study, we examined estrogen receptors (ER α and β) roles IOT, and it's relation to miR-21. Estrodiol (E2), PPT and DPN (ER α and β-specific agonists), as well as ER α- or ER β -specific shRNAs were applied to PA-1 IOT cells. We found E2/ER α signals promote cell migration and invasion through non-classical transactivation function. The data showed non-genomic E2/ER α activations of focal adhesion kinase-Ras homolog gene family member A (FAK-RhoA) and ERK governed cell mobility. The E2/ER α signaling induces epithelial-mesenchymal transition (EMT) and overexpression of CD133 through upregulation micro-RNA 21, and ERK phosphorylations. Knockdown of miR-21 in PA1 cells attenuated whereas overexpression of miR-21 promoted cell growth. Moreover, knockdown of miR-21 resulted in a marked reduction in the CD133+ population and sphere formation of CSPCs. In contrast, overexpression of miR-21 resulted in a marked increase in the population of CD133+ cells and sphere formation of CSPCs. Furthermore, E2/ER α signals trigger a positive feedback regulatory loop within miR21 and ERK. At last, cytosolic ER α, CD133, and EMT markers, but not epithelial cell markers, in IOT tissue samples were co-expressed. In conclusion, estrogenic signals exert malignant transformation capacity of cancer cells, exclusively through non-genomic regulation in female germ cell tumors.

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