Silencing of stathmin induces tumor-suppressor function in breast cancer cell lines harboring mutant p53

E. Alli, J. M. Yang, W. N. Hait

Research output: Contribution to journalArticlepeer-review

99 Scopus citations


Cancers harboring dominant-negative p53 mutations are often aggressive and difficult to treat. Direct attempts to restore wild-type p53 function have produced little clinical benefit. We investigated whether targeting a p53-target gene could induce certain tumor-suppressor characteristics. We found that inhibition of stathmin, a microtubule regulator that can be transcriptionally repressed by wild-type p53, restored certain wild-type functions to cancer cells with mutant p53. Silencing of stathmin by small interfering RNA (siRNA) in mutant p53 cell lines lowered expression to that observed following activation of wild-type p53 by DNA damage in wild-type p53 cell lines. siRNA-induced repression of stathmin decreased cell proliferation, viability and clonogenicity in mutant p53 cell lines. Furthermore, knockdown of stathmin partially restored cell-cycle regulation and activation of apoptosis. Therefore, targeting stathmin, a gene product that is overexpressed in the presence of mutant p53, may represent a novel approach to treating cancers with aberrant p53 function.

Original languageEnglish
Pages (from-to)1003-1012
Number of pages10
Issue number7
StatePublished - Feb 15 2007

Bibliographical note

Funding Information:
This work was supported by US Public Health Service NCI CA 78695 and CA 72720.


  • Apoptosis
  • Breast cancer
  • Cell-cycle arrest
  • Mitosis
  • Stathmin

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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