Stathmin, Interacting with Nf-κB, Promotes Tumor Growth and Predicts Poor Prognosis of Pancreatic Cancer

ISSN: 1875-5666 (Online)
ISSN: 1566-5240 (Print)

Volume 17, 10 Issues, 2017

Download PDF Flyer

Current Molecular Medicine

This journal supports open access

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 47th of 124 in Medicine, Research & Experimental

Submit Abstracts Online Submit Manuscripts Online

David W. Li
College of Medicine
University of Nebraska Medical Center
Omaha, NE

View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 2.912
5 - Year: 3.478

Stathmin, Interacting with Nf-κB, Promotes Tumor Growth and Predicts Poor Prognosis of Pancreatic Cancer

Current Molecular Medicine, 14(3): 328-339.

Author(s): Y. Lu, C. Liu, H. Cheng, Y. Xu, J. Jiang, J. Xu, J. Long, L. Liu and X Yu.

Affiliation: No. 270, Dong'An Road, Xuhui District, Shanghai, 200032, P.R. China.


Stathmin (STMN) has been known as a p53-regulated protein and has been shown to play an oncogenic role in a range of human malignancies. Paradoxically, most recent studies demonstrated that stathmin has a dual function as both an oncogene and a metastasis suppressor. Stathmin is a member of microtubule dynamic destabilizing proteins and stathmin-regulated microtubule disruption could lead to a variety of cell dysfunctions such as enhanced chronic hypoxia in pancreatic cancer. In this study, we identified that stathmin promotes proliferation of pancreatic cancer cells by an underlying nuclear factor kappa B (Nf-κB) interacting mechanism. In human specimens, stathmin was significantly overexpressed in pancreatic cancer tissues and high expression of stathmin was correlated with vascular emboli (p=0.028), tumor size (p=0.019), and overall survival (p=0.031). Functional assays showed that knockdown of stathmin significantly reduced pancreatic cancer cell viability, colony formation, and arrested the cell cycle at the G2/M phase. Furthermore, silence of stathmin could reduce pancreatic tumor growth in nude mice. For the mechanism, Western blot analyses demonstrated that Nf-κB (p65) was significantly down-regulated when stathmin was silenced. In addition, co-immunoprecipitation (CoIP) assay suggested that stathmin was able to interact with Nf-κB (p65). Our findings indicate that stathmin might play its oncogenic role by an interaction with Nf-κB pathway, which may reveal a novel mechanism to uncover the role of microtubule-destabilizing stathmin in pancreatic cancer environment as well as provide a potential therapeutic strategy for pancreatic cancer.


Nf-κB, pancreatic cancer, prognosis, stathmin, tumor growth.

Purchase Online Order Reprints Order Eprints Rights and Permissions

Article Details

Volume: 14
Issue Number: 3
First Page: 328
Last Page: 339
Page Count: 12
DOI: 10.2174/1566524014666140228120913
Price: $58

Related Journals

Webmaster Contact: Copyright © 2016 Bentham Science