Diverse matrix metalloproteinase functions regulate cancer amoeboid migration (Nature communication, 2014, 5:4255 :1-13)

報告日期: 2014/10/03
報告時間: 3:10/4:00
報告學生: 楊承翰
講評老師: 王育民
附件下載: 下載[1414-1411983106-1.pdf] 

Diverse matrix metalloproteinase functions

regulate cancer amoeboid migration

Jose L. Orgaz, Pahini Pandya, Rimple Dalmeida, Panagiotis Karagiannis, Berta Sanchez-Laorden,

Amaya Viros, Jean Albrengues, Frank O. Nestle, Anne J. Ridley, Cedric Gaggioli, Richard Marais,

Sophia N. Karagiannis2 & Victoria Sanz-Moreno

 

Nature Communications(2014) 5, 1–13

 

Speaker : Cheng-Han Yang (楊承翰)                        Time: 2014/10/03 15:10~16:00

Commentator : Yu-Ming Wang, Ph.D. (王育民 教授)           Room : 602

 

Abstract

Cancer metastasis is a complicated, multistep process. Before entering into the circulation system, tumor cells use migration and invasion in the tissues. It has been reported that rounded-amoeboid cells move faster than elongated-mesenchymal cells. However, the molecular mechanism of amoeboid cell migration is still obscure. In this paper, the authorsdemonstrated that amoeboid tumor cell-derived MMPs promote cell migration. They found MMP9 is highly expressed via Rho-ROCK and JAK-STAT3 pathway, and it promotes cell roundness and actomyosin contractilityindependent of catalytic activity. Moreover, they showed that CD44 functions as receptor for MMP9 in regulation of actomyosin contractility. In summary, these data indicated that MMP9 is a key regulator in amoeboid cell migration. This provided the value of the mechanism and lead to new strategy for anti-cancer therapy.

 

Referencesd

  1. Sanz-Moreno, V. et al. (2011) ROCK and JAK1 signaling cooperate to controlactomyosin contractility in tumor cells and stroma. Cancer Cell.20:229-245
  2. Friedl, P. & Wolf, K. (2003) Tumour-cell invasion and migration: diversity and escape

Mechanisms. Nat. Rev. Cancer. 3:362-374