AI Article Synopsis
- - The study investigates the role of the interferon-stimulated gene 15 (ISG15) pathway in breast cancer, revealing that it significantly alters cell structure and promotes migration in ZR-75-1 breast cancer cells.
- - ISG15 and its conjugating enzyme UbcH8 disrupt F-actin architecture and focal adhesions, which are critical for maintaining cell stability and shape.
- - The research indicates that ISG15 inhibits the breakdown of proteins related to tumor cell movement and invasion, suggesting that the ISG15 pathway could also affect similar processes in various other tumors beyond breast cancer.
Article Abstract
The interferon-stimulated gene 15 (ISG15) pathway is highly elevated in breast cancer; however, very little is known about how the ISG15 pathway contributes to breast tumorigenesis. In the current study, using the gene disruption approach, we demonstrate that both ISG15 and UbcH8 (ISG15-specific conjugating enzyme) disrupt F-actin architecture and formation of focal adhesions in ZR-75-1 breast cancer cells. In addition, ISG15 and UbcH8 promote breast cancer cell migration. We also demonstrate that ISG15 inhibits ubiquitin/26S proteasome-mediated turnover of proteins implicated in tumor cell motility, invasion and metastasis. Together, our results suggest that the aberrant activation of the ISG15 pathway confers a motile phenotype to breast cancer cells by disrupting cell architecture and stabilizing proteins involved in cell motility, invasion and metastasis. Because the cellular architecture is conserved and the ISG15 pathway is constitutively activated in tumor cells of different lineages, it is reasonable to assume that our observations in breast cancer must hold true for many other tumors.
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| http://dx.doi.org/10.1258/ebm.2011.011236 | DOI Listing |
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