The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
The activity status of cofilin is directly related to invasion, intravasation, and metastasis of mammary tumors
Open accessAbstract
Understanding the mechanisms controlling cancer cell invasion and metastasis constitutes a fundamental step in setting new strategies for diagnosis, prognosis, and therapy of metastatic cancers. LIM kinase1 (LIMK1) is a member of a novel class of serine–threonine protein kinases. Cofilin, a LIMK1 substrate, is essential for the regulation of actin polymerization and depolymerization during cell migration. Previous studies have made opposite conclusions as to the role of LIMK1 in tumor cell motility and metastasis, claiming either an increase or decrease in cell motility and metastasis as a result of LIMK1 over expression (Zebda, N., O. Bernard, M. Bailly, S. Welti, D.S. Lawrence, and J.S. Condeelis. 2000. J. Cell Biol. 151:1119–1128; Davila, M., A.R. Frost, W.E. Grizzle, and R. Chakrabarti. 2003. J. Biol. Chem. 278:36868–36875; Yoshioka, K., V. Foletta, O. Bernard, and K. Itoh. 2003. Proc. Natl. Acad. Sci. USA. 100:7247–7252; Nishita, M., C. Tomizawa, M. Yamamoto, Y. Horita, K. Ohashi, and K. Mizuno. 2005. J. Cell Biol. 171:349–359). We resolve this paradox by showing that the effects of LIMK1 expression on migration, intravasation, and metastasis of cancer cells can be most simply explained by its regulation of the output of the cofilin pathway. LIMK1-mediated decreases or increases in the activity of the cofilin pathway are shown to cause proportional decreases or increases in motility, intravasation, and metastasis of tumor cells.
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Cites
Gene expression profiling predicts clinical outcome of breast cancer
van 't Veer, L. J., Dai, H., van de Vijver, M. J., He, Y. D., Hart, A. A. M., Mao, M., Peterse, H. L., van der Kooy, K., Marton, M. J., Witteveen, A. T., et al. (2002) · Nature · doi:10.1038/415530a · Cited by 9,536
Cited by
Signaling mechanisms and functional roles of cofilin phosphorylation and dephosphorylation
Mizuno, K. (2013) · Cellular Signalling · doi:10.1016/j.cellsig.2012.11.001 · Cited by 396
Ins and outs of ADF/cofilin activity and regulation
Van Troys, M., Huyck, L., Leyman, S., Dhaese, S., Vandekerkhove, J., & Ampe, C. (2008) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2008.04.001 · Cited by 329
A Mena Invasion Isoform Potentiates EGF-Induced Carcinoma Cell Invasion and Metastasis
Philippar, U., Roussos, E. T., Oser, M., Yamaguchi, H., Kim, H.-D., Giampieri, S., Wang, Y., Goswami, S., Wyckoff, J. B., Lauffenburger, D. A., et al. (2008) · Developmental Cell · doi:10.1016/j.devcel.2008.09.003 · Cited by 269
Self-citationEGF-induced PIP2 hydrolysis releases and activates cofilin locally in carcinoma cells
van Rheenen, J., Song, X., van Roosmalen, W., Cammer, M., Chen, X., DesMarais, V., Yip, S.-C., Backer, J. M., Eddy, R. J., & Condeelis, J. S. (2007) · The Journal of Cell Biology · doi:10.1083/jcb.200706206 · Cited by 244
Self-citationGudheti, M. V., Curthoys, N. M., Gould, T. J., Kim, D., Gunewardene, M. S., Gabor, K. A., Gosse, J. A., Kim, C. H., Zimmerberg, J., & Hess, S. T. (2013) · Biophysical Journal · doi:10.1016/j.bpj.2013.03.054 · Cited by 106
Metadata
- Authors
- Wang, W., Mouneimne, G., Sidani, M., Wyckoff, J., Chen, X., Makris, A., Goswami, S., Bresnick, A. R., & Condeelis, J. S.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2006-05-01
- Volume
- 173
- Issue
- 3
- Pages
- 395-404
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2122693202
- Cited by
- 273
- References
- 1
- FWCI
- 8.74
- Type
- journal article
- Language
- en
- Open access
- green
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- Wang, W., Mouneimne, G., Sidani, M., Wyckoff, J., Chen, X., Makris, A., Goswami, S., Bresnick, A. R., & Condeelis, J. S. (2006). The activity status of cofilin is directly related to invasion, intravasation, and metastasis of mammary tumors. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200510115
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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