癌症研究
调解人
可药性
转移
生物
乳腺癌转移
乳腺癌
癌症
医学
癌症转移
基因
细胞生物学
遗传学
作者
Nir Ben‐Chetrit,David Chetrit,Roslin Russell,Cindy Körner,Maicol Mancini,Ali Abdul‐Hai,Tomer Itkin,Sílvia Carvalho,Hadas Cohen‐Dvashi,W. Koestler,Kirti Shukla,Moshit Lindzen,Merav Kedmi,Mattia Lauriola,Ziv Shulman,Haim Barr,Dalia Seger,Daniela A. Ferraro,Fresia Pareja,Hava Gil-Henn
出处
期刊:Science Signaling
[American Association for the Advancement of Science]
日期:2015-01-20
卷期号:8 (360): ra7-ra7
被引量:78
标识
DOI:10.1126/scisignal.2005537
摘要
Amplified HER2, which encodes a member of the epidermal growth factor receptor (EGFR) family, is a target of effective therapies against breast cancer. In search for similarly targetable genomic aberrations, we identified copy number gains in SYNJ2, which encodes the 5'-inositol lipid phosphatase synaptojanin 2, as well as overexpression in a small fraction of human breast tumors. Copy gain and overexpression correlated with shorter patient survival and a low abundance of the tumor suppressor microRNA miR-31. SYNJ2 promoted cell migration and invasion in culture and lung metastasis of breast tumor xenografts in mice. Knocking down SYNJ2 impaired the endocytic recycling of EGFR and the formation of cellular lamellipodia and invadopodia. Screening compound libraries identified SYNJ2-specific inhibitors that prevented cell migration but did not affect the related neural protein SYNJ1, suggesting that SYNJ2 is a potentially druggable target to block cancer cell migration.
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