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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 increased metastasis in vivo(A) Representative images of metastatic spread within the abdomen after orthotopic implantation of MIA, EV-MIA, and CD133hi-MIA cells. (B) H&E –stained sections of the spleen.
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Figure 4: CD133 expression increased metastasis in vivo(A) Representative images of metastatic spread within the abdomen after orthotopic implantation of MIA, EV-MIA, and CD133hi-MIA cells. (B) H&E –stained sections of the spleen.

Mentions: To determine the effect of CD133 expression on metastasis in vivo, CD133hi-MIA and EV-MIA cells were implanted orthotopically into the tail of the pancreas. Tumor growth was evident in all mice of each group; however, the site and spread of metastasis varied between groups (Table 2). Metastasis to spleen (4/10, 2/10, and 10/10 in MIA, EV-MIA, and CD133hi-MIA, respectively), lymph nodes (1/10, 0/10, and 10/10), liver (0/10, 0/10, and 6/10), abdominal wall (1/10, 0/10, and 8/10) and diaphragm (0/10, 0/10, and 5/10) increased upon overexpression of CD133 as compared with the MIA and EV-MIA controls (Table 2 and Figure 4A, 4B).


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 increased metastasis in vivo(A) Representative images of metastatic spread within the abdomen after orthotopic implantation of MIA, EV-MIA, and CD133hi-MIA cells. (B) H&E –stained sections of the spleen.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: CD133 expression increased metastasis in vivo(A) Representative images of metastatic spread within the abdomen after orthotopic implantation of MIA, EV-MIA, and CD133hi-MIA cells. (B) H&E –stained sections of the spleen.
Mentions: To determine the effect of CD133 expression on metastasis in vivo, CD133hi-MIA and EV-MIA cells were implanted orthotopically into the tail of the pancreas. Tumor growth was evident in all mice of each group; however, the site and spread of metastasis varied between groups (Table 2). Metastasis to spleen (4/10, 2/10, and 10/10 in MIA, EV-MIA, and CD133hi-MIA, respectively), lymph nodes (1/10, 0/10, and 10/10), liver (0/10, 0/10, and 6/10), abdominal wall (1/10, 0/10, and 8/10) and diaphragm (0/10, 0/10, and 5/10) increased upon overexpression of CD133 as compared with the MIA and EV-MIA controls (Table 2 and Figure 4A, 4B).

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