Networks of E-cadherin, β1 integrin, and focal adhesion kinase in the pathogenesis of tubal pregnancy.

E-cadherin, β1 integrin, and focal adhesion kinase (FAK) are reported to involved in eutopic implantation by mediating cell adhesion. However, less is documented about their roles in ectopic implantation. This study was undertaken to evaluate the roles and networks of E-cadherin, β1 integrin, and FAK in tubal pregnancy. A total of 31 Fallopian tube specimens were obtained from tubal pregnant women. Immunohistochemistry and western blot were used to analyze the distributions and levels of E-cadherin, β1 integrin and phosphorylated-FAK (Pho-FAK) in the Fallopian tube epithelium. Normal Fallopian tube samples derived from non-pregnant women with benign genital diseases were used for comparison. E-cadherin presented in the cytomembrane of tubal epithelial cells and β1 integrin mainly expressed in the cytoplasm. A lowest-level of E-cadherin was detected in the implantation site (0.63 ± 0.29) when compared with the non-implantation site (0.95 ± 0.37) and the controls (0.89 ± 0.33) (P < 0.05). β1 integrin, as well as Pho-FAK in the implantation site (0.81 ± 0.35; 0.72 ± 0.24), showed a higher-level than that in the non-implantation site (0.59 ± 0.26; 0.48 ± 0.27) or the control group (0.38 ± 0.19; 0.36 ± 0.25) (p < .05). The decreased E-cadherin and increased β1 integrin are implicated in tubal pregnancy. The involvement of β1 integrin maybe depends on β1 integrin/FAK signaling.