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BMC Cancer. 2015 Apr 11;15:266. doi: 10.1186/s12885-015-1251-8.

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

Author information

1
Department of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. cpasiliao@gmail.com.
2
Department of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. chewei68@hotmail.com.
3
Department of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. bsutherland@bccrc.ca.
4
Department of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. svaldez@bccrc.ca.
5
Department of Pathology and Laboratory Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC, V6T 2B5, Canada. david.schaeffer@vch.ca.
6
The Pancreas Centre BC, 2775 Laurel St., Vancouver, BC, V5Z 1M9, Canada. david.schaeffer@vch.ca.
7
Department of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. dyapp@bccrc.ca.
8
The Pancreas Centre BC, 2775 Laurel St., Vancouver, BC, V5Z 1M9, Canada. dyapp@bccrc.ca.
9
Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. dyapp@bccrc.ca.
10
Department of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. sylvia.ng@rmp.uhn.ca.
11
Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. sylvia.ng@rmp.uhn.ca.

Abstract

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.

PMID:
25886367
PMCID:
PMC4403680
DOI:
10.1186/s12885-015-1251-8
[Indexed for MEDLINE]
Free PMC Article

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