Cell adhesion has an essential role in regulating metastasis, and loss of cell adhesion is a classic feature of invasion. There is currently a great deal of interest in the role of adhesion proteins and the antimetastatic protein nm23H1 in the progression of cancer. However, reports on the expression of these proteins in complete hydatidiform moles (CHMs) are limited. In the present study, expression of the adhesion molecules E-cadherin, P-cadherin, CD44, and CD44v6, and the antimetastatic protein nm23H1 was assessed in relation to the invasive potential of CHMs. This is the first report on the expression of these proteins in CHMs. Immunohistochemical assessment was carried out in CHMs (105 cases including 15 cases of invasive moles) and compared with that of gestational age-matched normal placentae (95 cases). The expression of the adhesion proteins ranged from mild to moderate intensity with a general down-regulation in the molar trophoblasts, the down-regulation in CD44 and CD44V6 being highly significant. No relation was, however, noticed with the invasiveness or the persistence of the disease. nm23H1 protein, on the other hand, was significantly down-regulated in the molar trophoblasts with none of the invasive lesions showing intense expression. The study thus suggests down-regulation of adhesion proteins, especially that of CD44 and CD44v6, to be an early step in the transformation to molar placenta with reduced expression of nm23H1 conferring an invasive potential to the trophoblasts.

nm23-H1 expression could be used as a marker for accurate evaluation of myometrial invasion in complete hydatidiform mole.

nm23-H1 expression could be used as a marker for accurate evaluation of myometrial invasion in complete hydatidiform mole.