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      Alterations in mechanical properties are associated with prostate cancer progression.

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          Abstract

          Cancer progression and metastasis have been shown to be accompanied by alterations in the mechanical properties of tissues, but the relationship between the mechanical properties and malignant behavior in prostate cancer (Pca) is less clear. The aims of this study were to detect the mechanical properties of benign prostatic hyperplasia (BPH) and Pca tissues on both the macro- and micro-scales, to explore the relationships between mechanical properties and malignant behavior and, finally, to identify the important molecules in the mechanotransduction signaling pathway. We demonstrated that the strain index of Pca tissue was significantly higher than that of BPH tissue on the macro-scale but the Young's modulus of the Pca tissues, especially in advanced Pca, was lower than that of BPH tissues on the micro-scale. These two seemingly contradictory results can be explained by the excessive proliferation of tumor cells (Ki-67) and the degradation of scaffold proteins (collagens). These data indicate that alterations of the macro- and micro-mechanical properties of Pca tissues with malignant behavior are contradictory. The mechanical properties of tissues might be useful as a new risk factor for malignancy and metastasis in Pca. Furthermore, collagens, matrix metalloproteinase, fibronectin, and integrins might be the important molecules in the mechanotransduction signaling pathway.

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          Author and article information

          Journal
          Med. Oncol.
          Medical oncology (Northwood, London, England)
          Springer Nature
          1559-131X
          1357-0560
          Mar 2014
          : 31
          : 3
          Affiliations
          [1 ] Department of Urology, First Affiliated Hospital of Dalian Medical University, Zhongshan Road No. 222, Dalian, 116011, China.
          Article
          10.1007/s12032-014-0876-9
          24504844
          5631c6b8-1b34-43c6-b1b5-395067344169
          History

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