| First Author | Faraldo ML | Year | 1997 |
| Journal | Mol Carcinog | Volume | 20 |
| Issue | 1 | Pages | 33-47 |
| PubMed ID | 9328434 | Mgi Jnum | J:43947 |
| Mgi Id | MGI:1099169 | Doi | 10.1002/(sici)1098-2744(199709)20:1<33::aid-mc5>3.0.co;2-j |
| Citation | Faraldo ML, et al. (1997) Analysis of the E-cadherin and P-cadherin promoters in murine keratinocyte cell lines from different stages of mouse skin carcinogenesis. Mol Carcinog 20(1):33-47 |
| abstractText | We previously isolated the 5' upstream sequences of the mouse P-cadherin gene, in which putative binding sites for several transcription factors were identified between nt-101 and +30. In the study reported here, the promoter activity of the postulated 5' cis-acting sequences of the P-cadherin promoter, and the activity of the proximal E-cadherin promoter were investigated in several murine keratinocyte cell lines showing different levels of P- and E-cadherin expression as well as different morphology and tumorigenic behavior. Cell-type specificity and optimal activity of P-cadherin expression in murine keratinocytes was conferred by 5' sequences located between nt -200 and +30, and the GC-rich region (nt -101 to +80) and a CCAAT box element (nt -65) had a major regulatory role. The cell-type specificity of the E-cadherin promoter, on the other hand, was mediated by a combination of positive regulatory elements, a GC-rich region (nt -58 to -24), and a CCAAT box (nt -65) and repressor elements inside the E-pal sequence. Interestingly, the maximum repressor effect of the E-pal element was observed in non-expressing undifferentiated spindle cells. In vitro binding studies indicated that the GC-rich region of the P-cadherin promoter was mainly recognized by Sp1-related nuclear factors, whereas both AP2- and Sp1-related factors were involved in the interaction of the GC-rich region of the E-cadherin promoter. Common factors (probably related to the CP1 family) seemed also to be involved in the recognition of the CCAAT-box element of both the E- and P-cadherin promoters, but additional specific factors participated in the interaction with the CCAAT box of the E-cadherin promoter. Our studies also support the hypothesis that loss or modification of some of the regulatory factors occurs during mouse skin tumor progression. |
