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Cell Death and Disease:厦门大学药学院王团老教授课题组发表肿瘤研究文章

摘要 : 2015年10月15日,Nature出版集团旗下子刊《Cell Death&Disease》期刊上在线发表了厦门大学药学院王团老教授课题组的一项研究文章,文章揭示囊泡运输通过信号传导影响细胞迁移、侵袭和肿瘤发生的机制

 2015年10月15日,Nature出版集团旗下子刊《Cell Death&Disease》期刊上在线发表了厦门大学药学院王团老教授课题组的一项研究文章,文章揭示囊泡运输通过信号传导影响细胞迁移、侵袭和肿瘤发生的机制,文章题为“RILP suppresses invasion of breast cancer cells by modulating the activity of RalA through interaction with RalGDS”。


图 RILP与RalGDS互作抑制细胞侵袭的机制


RILP suppresses invasion of breast cancer cells by modulating the activity of RalA through interaction with RalGDS


RILP (Rab7-interacting lysosomal protein) is a key regulator for late endosomal/lysosomal trafficking, and probably a tumor suppressor in prostate cancer. However, the role of RILP in other cancers and the underlying mechanism for RILP in regulating the invasion of cancer cells remain to be investigated. In this study, we showed that overexpression of RILP in breast cancer cells inhibits the migration and invasion, wheras the depletion of RILP by RNAi-mediated knockdown promotes the migration and invasion. We identified RalGDS (Ral guanine nucleotide dissociation stimulator) as a novel interacting partner for RILP, and truncation analysis revealed the N-terminal region of RILP is responsible for interacting with the guanine nucleotide exchange factor (GEF) domain of RalGDS. Immunofluorescence microscopy revealed that RalGDS can be recruited to the late endosomal compartments by RILP. Further investigations indicated that the overexpression of RILP inhibits the activity of RalA, a downstream target of RalGDS. Our data suggest that RILP suppresses the invasion of breast cancer cells by interacting with RalGDS to inhibit its GEF activity for RalA.

来源: Cell Death&Disease 浏览次数:0


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