Mechanical phenotype of cancer cells: Cell softening and loss of stiffness sensing

Hsi Hui Lin, Hsiu Kuan Lin, I. Hsuan Lin, Yu Wei Chiou, Horn Wei Chen, Ching Yi Liu, Hans I.Chen Harn, Wen Tai Chiu, Yang Kao Wang, Meng Ru Shen, Ming Jer Tang

研究成果: Article同行評審

124 引文 斯高帕斯(Scopus)

摘要

The stiffness sensing ability is required to respond to the stiffness of the matrix. Here we determined whether normal cells and cancer cells display distinct mechanical phenotypes. Cancer cells were softer than their normal counterparts, regardless of the type of cancer (breast, bladder, cervix, pancreas, or Ha-RasV12-transformed cells). When cultured on matrices of varying stiffness, low stiffness decreased proliferation in normal cells, while cancer cells and transformed cells lost this response. Thus, cancer cells undergo a change in their mechanical phenotype that includes cell softening and loss of stiffness sensing. Caveolin-1, which is suppressed in many tumor cells and in oncogene-transformed cells, regulates the mechanical phenotype. Caveolin-1- upregulated RhoA activity and Y397FAK phosphorylation directed actin cap formation, which was positively correlated with cell elasticity and stiffness sensing in fibroblasts. Ha-RasV12-induced transformation and changes in the mechanical phenotypes were reversed by re-expression of caveolin-1 and mimicked by the suppression of caveolin-1 in normal fibroblasts. This is the first study to describe this novel role for caveolin-1, linking mechanical phenotype to cell transformation. Furthermore, mechanical characteristics may serve as biomarkers for cell transformation.

原文English
頁(從 - 到)20946-20958
頁數13
期刊Oncotarget
6
發行號25
DOIs
出版狀態Published - 2015

All Science Journal Classification (ASJC) codes

  • 腫瘤科

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