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.KeywordsFluorescence Resonance Energy TransferCancer Cell SensitivityNeuronal Progenitor CellQ18E MutationTubulin mRNAThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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