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2016 ; 7
(45
): 73725-73738
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Role of BCL9L in transforming growth factor-? (TGF-?)-induced
epithelial-to-mesenchymal-transition (EMT) and metastasis of pancreatic cancer
#MMPMID27713160
Sannino G
; Armbruster N
; Bodenhöfer M
; Haerle U
; Behrens D
; Buchholz M
; Rothbauer U
; Sipos B
; Schmees C
Oncotarget
2016[Nov]; 7
(45
): 73725-73738
PMID27713160
show ga
Pancreatic ductal adenocarcinoma (PDAC) has a low overall survival rate, which is
approximately 20% during the first year and decreases to less than 6% within five
years of the disease. This is due to premature dissemination accompanied by a
lack of disease-specific symptoms during the initial stages. Additionally, to
date there are no biomarkers for an early prognosis available.A growing number of
studies indicate that epithelial to mesenchymal transition (EMT), triggered by
WNT-, TGF-?- and other signaling pathways is crucial for the initiation of the
metastatic process in PDAC. Here we show, that BCL9L is up-regulated in PDAC cell
lines and patient tissue compared to non-cancer controls. RNAi-induced BCL9L
knockdown negatively affected proliferation, migration and invasion of pancreatic
cancer cells. On a molecular basis, BCL9L depletion provoked an increment of
E-cadherin protein levels, with concomitant increase of ?-catenin retention at
the plasma membrane. This is linked to the induction of a strong epithelial
phenotype in pancreatic cancer cells upon BCL9L knockdown even in the presence of
the EMT-inducer TGF-?. Finally, xenograft mouse models of pancreatic cancer
revealed a highly significant reduction in the number of liver metastases upon
BCL9L knockdown. Taken together, our findings underline the key importance of
BCL9L for EMT and thus progression and metastasis of pancreatic cancer cells.
Direct targeting of this protein might be a valuable approach to effectively
antagonize invasion and metastasis of PDAC.
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