News Release

LIMK plays a key role in cancer metastasis

Peer-Reviewed Publication

Rockefeller University Press

Researchers have shown that LIM kinase (LIMK), an important regulator of actin cytoskeleton dynamics, plays a key role in cancer metastasis. The study appears online on September 27 in The Journal of Cell Biology www.jcb.org.

Cancer metastasis is a multi-stage process that starts with the invasion of tumor cells into their surrounding tissue. The ability of metastatic cells to invade requires reorganization of the actin-myosin cytoskeleton, which is controlled by a sophisticated network of signals sent between a number of cellular components.

LIMK has been shown previously to facilitate tumor invasion through its role in actin regulation. Researchers from the United Kingdom delved deeper into the role of LIMK in this process. The team showed that LIMK is specifically required for cells at the front of the invading tumor to clear a path that the remaining metastatic cells can follow. Working with breast cancer and squamous carcinoma cells, the team found that inhibiting LIMK function blocked the collective invasion of tumor cells, thus preventing these cells from metastasizing.

The authors propose that LIMK inhibitors might be effective in the treatment of cancers such as prostate cancer, where the presence of localized tumors might not be life threatening but mortality can result from metastasis.

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About The Journal of Cell Biology

Founded in 1955, The Journal of Cell Biology (JCB) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JCB content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit www.jcb.org.

Scott, R.W., et al. 2010. J. Cell Biol. doi:10.1083/jcb.201002041.


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