Reduced expression of neural cell adhesion molecule induces metastatic dissemination of pancreatic β tumor cells
As in the development of many human cancers, in a transgenic mouse model of β-cell
carcinogenesis (Rip1Tag2), expression of neural cell adhesion molecule (NCAM) changes
from the 120-kDa isoform in normal tissue to the 140/180-kDa isoforms in tumors. NCAM-
deficient Rip1Tag2 mice, generated by crossing Rip1Tag2 mice with NCAM knockout mice,
develop metastases, a tumor stage that is not seen in normal Rip1Tag2 mice. In contrast,
overexpression of NCAM 120 in NCAM-deficient Rip1Tag2 mice prevents tumor metastasis …
carcinogenesis (Rip1Tag2), expression of neural cell adhesion molecule (NCAM) changes
from the 120-kDa isoform in normal tissue to the 140/180-kDa isoforms in tumors. NCAM-
deficient Rip1Tag2 mice, generated by crossing Rip1Tag2 mice with NCAM knockout mice,
develop metastases, a tumor stage that is not seen in normal Rip1Tag2 mice. In contrast,
overexpression of NCAM 120 in NCAM-deficient Rip1Tag2 mice prevents tumor metastasis …
Abstract
As in the development of many human cancers, in a transgenic mouse model of β-cell carcinogenesis (Rip1Tag2), expression of neural cell adhesion molecule (NCAM) changes from the 120-kDa isoform in normal tissue to the 140/180-kDa isoforms in tumors. NCAM-deficient Rip1Tag2 mice, generated by crossing Rip1Tag2 mice with NCAM knockout mice, develop metastases, a tumor stage that is not seen in normal Rip1Tag2 mice. In contrast, overexpression of NCAM 120 in NCAM-deficient Rip1Tag2 mice prevents tumor metastasis. The results indicate that the loss of NCAM-mediated cell adhesion is one rate-limiting step in the actual metastatic dissemination of β tumor cells.
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