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CD133 initiates tumors, induces epithelial-mesenchymal transition and increases metastasis in pancreatic cancer.

Nomura A, Banerjee S, Chugh R, Dudeja V, Yamamoto M, Vickers SM, Saluja AK - Oncotarget (2015)

Bottom Line: Additionally, CD133 expression induced epithelial-mesenchymal transition (EMT) and increased in vitro invasion.EMT induction and increased invasiveness were mediated by NF-κB activation, as inhibition of NF-κB mitigated these effects.This study showed that CD133 expression contributes to pancreatic cancer "stemness," tumorigenicity, EMT induction, invasion, and metastasis.

View Article: PubMed Central - PubMed

Affiliation: Division of Basic and Translational Research, Department of Surgery, University of Minnesota, Minneapolis, MN, USA.

ABSTRACT
CD133 has been implicated as a cancer stem cell (CSC) surface marker in several malignancies including pancreatic cancer. However, the functional role of this surface glycoprotein in the cancer stem cell remains elusive. In this study, we determined that CD133 overexpression induced "stemness" properties in MIA-PaCa2 cells along with increased tumorigenicity, tumor progression, and metastasis in vivo. Additionally, CD133 expression induced epithelial-mesenchymal transition (EMT) and increased in vitro invasion. EMT induction and increased invasiveness were mediated by NF-κB activation, as inhibition of NF-κB mitigated these effects. This study showed that CD133 expression contributes to pancreatic cancer "stemness," tumorigenicity, EMT induction, invasion, and metastasis.

No MeSH data available.


Related in: MedlinePlus

CD133 expression induces EMT and increases invasiveness in vitro(A)In vitro Boyden chamber invasion of MIA, EV-MIA, CD133hi-MIA with representative images from the Boyden chamber invasion assay, (B) Invasion upon CD133 silencing in CD133hi-MIA with representative images, and (C) EMT gene expression in CD133hi-MIA as compared with EV-MIA control and protein expression of Vimentin and N-Cadherin.
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Figure 3: CD133 expression induces EMT and increases invasiveness in vitro(A)In vitro Boyden chamber invasion of MIA, EV-MIA, CD133hi-MIA with representative images from the Boyden chamber invasion assay, (B) Invasion upon CD133 silencing in CD133hi-MIA with representative images, and (C) EMT gene expression in CD133hi-MIA as compared with EV-MIA control and protein expression of Vimentin and N-Cadherin.

Mentions: Our recent data indicated that CD133 expression correlated with the invasive ability of the cells. To determine if CD133 overexpression indeed led to increased invasiveness in MIA PaCa-2 cells, we performed a Boyden chamber invasion assay. The number of CD133hi-MIA cells invading the Matrigel membrane was 5.9 fold greater as compared with the MIA and EV-MIA controls (Figure 3A). These results were validated when knockdown of CD133 using CD133-specific siRNA (Supplementary Figure 1C) in CD133hi-MIA resulted in a significant decrease in invasion, compared with CD133hi-non-silencing controls (Figure 3B). As seen with stemness properties, the invasive property of clones correlated with their CD133 expression (Supplementary Figure 5C).


CD133 initiates tumors, induces epithelial-mesenchymal transition and increases metastasis in pancreatic cancer.

Nomura A, Banerjee S, Chugh R, Dudeja V, Yamamoto M, Vickers SM, Saluja AK - Oncotarget (2015)

CD133 expression induces EMT and increases invasiveness in vitro(A)In vitro Boyden chamber invasion of MIA, EV-MIA, CD133hi-MIA with representative images from the Boyden chamber invasion assay, (B) Invasion upon CD133 silencing in CD133hi-MIA with representative images, and (C) EMT gene expression in CD133hi-MIA as compared with EV-MIA control and protein expression of Vimentin and N-Cadherin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4480754&req=5

Figure 3: CD133 expression induces EMT and increases invasiveness in vitro(A)In vitro Boyden chamber invasion of MIA, EV-MIA, CD133hi-MIA with representative images from the Boyden chamber invasion assay, (B) Invasion upon CD133 silencing in CD133hi-MIA with representative images, and (C) EMT gene expression in CD133hi-MIA as compared with EV-MIA control and protein expression of Vimentin and N-Cadherin.
Mentions: Our recent data indicated that CD133 expression correlated with the invasive ability of the cells. To determine if CD133 overexpression indeed led to increased invasiveness in MIA PaCa-2 cells, we performed a Boyden chamber invasion assay. The number of CD133hi-MIA cells invading the Matrigel membrane was 5.9 fold greater as compared with the MIA and EV-MIA controls (Figure 3A). These results were validated when knockdown of CD133 using CD133-specific siRNA (Supplementary Figure 1C) in CD133hi-MIA resulted in a significant decrease in invasion, compared with CD133hi-non-silencing controls (Figure 3B). As seen with stemness properties, the invasive property of clones correlated with their CD133 expression (Supplementary Figure 5C).

Bottom Line: Additionally, CD133 expression induced epithelial-mesenchymal transition (EMT) and increased in vitro invasion.EMT induction and increased invasiveness were mediated by NF-κB activation, as inhibition of NF-κB mitigated these effects.This study showed that CD133 expression contributes to pancreatic cancer "stemness," tumorigenicity, EMT induction, invasion, and metastasis.

View Article: PubMed Central - PubMed

Affiliation: Division of Basic and Translational Research, Department of Surgery, University of Minnesota, Minneapolis, MN, USA.

ABSTRACT
CD133 has been implicated as a cancer stem cell (CSC) surface marker in several malignancies including pancreatic cancer. However, the functional role of this surface glycoprotein in the cancer stem cell remains elusive. In this study, we determined that CD133 overexpression induced "stemness" properties in MIA-PaCa2 cells along with increased tumorigenicity, tumor progression, and metastasis in vivo. Additionally, CD133 expression induced epithelial-mesenchymal transition (EMT) and increased in vitro invasion. EMT induction and increased invasiveness were mediated by NF-κB activation, as inhibition of NF-κB mitigated these effects. This study showed that CD133 expression contributes to pancreatic cancer "stemness," tumorigenicity, EMT induction, invasion, and metastasis.

No MeSH data available.


Related in: MedlinePlus