CDH-16/Ksp-cadherin was first described as a kidney-specific adhesion molecule belonging to the 7-D cadherin family. A binding partner of its cytosolic domain, alpha B-crystallin, that possibly mediates the connection to the actin cytoskeleton, was recently identified. We determined by microarray analysis that CDH-16 and alpha B-crystallin genes are expressed in the thyroid. CDH-16 was expressed in the mouse thyroid already at E15 and, by confocal microscopy, it co-localized with E-cadherin. In thyroid cell cultures, the expression of CDH-16 was hormone dependent as most thyroid differentiation markers. In human thyroid tumors CDH-16 and E-cadherin were progressively lost from the plasma membrane and a marked decrease in their expression was observed by RT-PCR. A marked decrease of the alpha B-crystallin gene expression was also observed. By TMA and by confocal microscopy all E-cadherin-negative tumor cells were also negative for CDH-16. However, E-cadherin-positive cells were often negative for CDH-16 indicating that the latter is the first to be lost during tumor progression. Our working hypothesis is that CDH-16 plays a role in thyroid cell differentiation and transformation.

CDH-16 gene expression in thyroid cell differentiation and transformation

PALLANTE, PIERLORENZO;FUSCO, ALFREDO;NITSCH, LUCIO
2008

Abstract

CDH-16/Ksp-cadherin was first described as a kidney-specific adhesion molecule belonging to the 7-D cadherin family. A binding partner of its cytosolic domain, alpha B-crystallin, that possibly mediates the connection to the actin cytoskeleton, was recently identified. We determined by microarray analysis that CDH-16 and alpha B-crystallin genes are expressed in the thyroid. CDH-16 was expressed in the mouse thyroid already at E15 and, by confocal microscopy, it co-localized with E-cadherin. In thyroid cell cultures, the expression of CDH-16 was hormone dependent as most thyroid differentiation markers. In human thyroid tumors CDH-16 and E-cadherin were progressively lost from the plasma membrane and a marked decrease in their expression was observed by RT-PCR. A marked decrease of the alpha B-crystallin gene expression was also observed. By TMA and by confocal microscopy all E-cadherin-negative tumor cells were also negative for CDH-16. However, E-cadherin-positive cells were often negative for CDH-16 indicating that the latter is the first to be lost during tumor progression. Our working hypothesis is that CDH-16 plays a role in thyroid cell differentiation and transformation.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/341587
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