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Stathmin and Cancer

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Cytoskeleton and Human Disease

Abstract

Stathmin (STMN) is an evolutionarily conserved, ubiquitously expressed, tubulin-binding protein that has been associated with cell proliferation and differentiation. The widely reported over-expression of STMN in human malignancies suggests significant function in cancer and may represent a viable target to reduce disease. We discuss the transcriptional and post-transcriptional regulation of STMN expression and review the complex signalling networks that impact STMN activity through post-translational modification and protein interactions. Recent advances have also revealed STMN contributions towards chromosome instability leading to aneuploidy, cell migration/invasion and chemoresistance. These studies highlight that STMN potentially contributes to tumour development and progression through the regulation of multiple cellular processes. Reports of STMN interaction with anti-cancer drugs have also provided new insights on STMN mechanisms in drug-refractory malignancies and highlighted the potential of combining STMN inhibition with established therapies. These advances provide fundamental information necessary to evaluate the therapeutic value of targeting STMN in the treatment of cancer.

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Acknowledgments

We would like to thank Marie Bogoyevitch for helpful suggestions in editing. Research by the authors on STMN function and regulation has been supported by the Australian National Health and Medical Research Council (628335). D.C.H. Ng is also supported by the MDHS CR Roper Fellowship and Frances Byrne by an Anthony Rothe Postgraduate Scholarship.

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Correspondence to Dominic Chi Hiung Ng .

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Ng, D., Byrne, F. (2012). Stathmin and Cancer. In: Kavallaris, M. (eds) Cytoskeleton and Human Disease. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-61779-788-0_14

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