Research Of Notch Signaling Pathway Mediated-epithelial-to-mesenchymal Transition In Regulation Of Breast Cancer Development

Objective: To investigate the expression of Notch signaling molecular and EMT in invasive ductalcarcinoma (IDC), ductal carcinoma in situ (DCIS), usual ductal hyperplasia (UDH) and normal-cancerousadjacent tissue (NCAT), then analyze the relationship between Notch1and EMT expression andtumorigenesis and invasion.Methods: Immunohistochemistry Envision was used to examine the expressions ofNotch1,E-cadherin,N-cadherin,vimentin in254patients with IDC,32patients with DCIS,40patients withUDH and37cases of NCAT, which was further to investigate the association of Notch1and EMTexpression and breast cancer development.Results:①The positive percentage of Notch1expression in UDH,DCIS, IDC, and UDH were7.5%,84.3%,84.0%,48.6%,respectively, that of E-cadherin expression were82.5%,56.3%,48.5%,81.1%,that of N-cadherin expression were35.0%,78.1%,94.5%,81.1%, and Vimentin expressionwere12.5%,12.5%,11.5%,2.7%.②A significance was observed between DCIS, UDH and NCAT, andranging from UDH to DCIS and then IDC, Notch1expression was gradually increased with an increasinglyelevated expression of N-cadherin and a gradual reduction of E-cadherin.③A significantly negativerelation was found between E-cadherin and N-cadherin(r=-0.205, P=0.004), and a significantly positiverelation was revealed between Notch1and E-cadherin expression(r=0.247，p=0.001).Conclusions:1EMT in mammary epithelial cells might cooperate with tumorigenesis and invasion tosome extent.2Notch1induced-EMT facilitated the invasion of breast carcinoma, which was verified inparaffin-embedded tissue, and the presumption that the enhancement of EMT induced by high Notch1expression in cancer cells was achieved by promoting the expression of N-cadherin remained to be furtherconfirmed.