Special AT-rich sequence-binding protein 2 suppresses invadopodia formation in HCT116 cells via palladin inhibition

Mohammed A. Mansour, Eri Asano, Toshinori Hyodo, K. A. Akter, Masahide Takahashi, Michinari Hamaguchi, Takeshi Senga

研究成果: ジャーナルへの寄稿学術論文査読

13 被引用数 (Scopus)

抄録

Invadopodia are specialized actin-based microdomains of the plasma membrane that combine adhesive properties with matrix degrading activities. Proper functioning of the bone, immune, and vascular systems depend on these organelles, and their relevance in cancer cells is linked to tumor metastasis. The elucidation of the mechanisms driving invadopodia formation is a prerequisite to understanding their role and ultimately to controlling their functions. Special AT-rich sequence-binding protein 2 (SATB2) was reported to suppress tumor cell migration and metastasis. However, the mechanism of action of SATB2 is unknown. Here, we show that SATB2 inhibits invadopodia formation in HCT116 cells and that the molecular scaffold palladin is inhibited by exogenous expression of SATB2. To confirm this association, we elucidated the function of palladin in HCT116 using a knock down strategy. Palladin knock down reduced cell migration and invasion and inhibited invadopodia formation. This phenotype was confirmed by a rescue experiment. We then demonstrated that palladin expression in SATB2-expressing cells restored invasion and invadopodia formation. Our results showed that SATB2 action is mediated by palladin inhibition and the SATB2/palladin pathway is associated with invadopodia formation in colorectal cancer cells.

本文言語英語
ページ(範囲)78-88
ページ数11
ジャーナルExperimental Cell Research
332
1
DOI
出版ステータス出版済み - 01-03-2015
外部発表はい

All Science Journal Classification (ASJC) codes

  • 細胞生物学

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