The involvement of insulin-like growth factor 2 binding protein 3 (IMP3) in pancreatic cancer cell migration, invasion, and adhesion

BMC Cancer

Clarissa C Pasiliao¹  Che-Wei A Chang¹  Brent W Sutherland¹  Shannon M Valdez¹  David Schaeffer³  Donald T Yapp²  Sylvia S W Ng² 

[1] Department of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver V5Z 1 L3, BC, Canada

[2] Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver V6T 1Z3, BC, Canada

[3] The Pancreas Centre BC, 2775 Laurel St., Vancouver V5Z 1M9, BC, Canada

关键词: Adhesion;    Invasion;    Motility;    mRNA binding;    Pancreatic ductal adenocarcinoma;   

Others  :  1171687
DOI  :  10.1186/s12885-015-1251-8

 received in 2013-08-31, accepted in 2015-03-25,  发布年份 2015

【 摘 要 】

Background

Over-expression of insulin-like growth factor 2 mRNA binding protein 3 (IMP3) is correlated with poor prognosis in pancreatic ductal adenocarcinoma (PDAC). Previous studies examining other cancer types have implicated IMP3 in the regulation of several cellular functions that are characteristic of tumour cells. However, the role of this oncofetal protein in PDAC progression remained unclear.

Methods

Using siRNA, we examined the effect of IMP3 inhibition on the motility, invasive ability, and matrix adhesion of PDAC cells. In addition, we also evaluated the expression of cytoskeleton-associated genes following IMP depletion.

Results

Knockdown of IMP3 significantly decreased the motility, invasion, and extracellular matrix adhesion of select PDAC cells in vitro. In addition, IMP3-depleted cells exhibited lower levels of CD44 protein and KIF11 mRNA. Moreover, we also observed a reduction in downstream RhoA signaling following IMP3 knockdown, indicating that IMP3 modulates the levels of proteins involved in cytoskeletal organization.

Conclusions

These results suggest that IMP3 facilitates PDAC progression by enhancing the pro-metastatic behaviour of tumour cells.

【 授权许可】

   
2015 Pasiliao et al.; licensee BioMed Central.

【 图 表 】

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