1A and B), but protein expression of E-cadherin
was decreased by E2, BPA, or NP about 20% than that by a control (p < 0.
, which inhibits cancer cell migration and invasion, was reduced in B[a] P-treated groups relative to the control group, but expression of metastasis-promoting proteins, including N-cadherin, vimentin, snail, and slug, were induced after B[a]P exposure (Figure 2F).
Negative expression of the epithelial calcium-dependent adhesion molecule E-cadherin
has been shown to be a sensitive and specific biomarker to confirm the invasive lobular carcinoma subtype among tumors with histologically equivocal features (18, 19).
The dietary phytochemical chlorophyllin alters E-cadherin
and beta-catenin expression in human colon cancer cells.
Immunohistochemical staining of oncocytoma areas (A) Positive E-cadherin
Aberrant expression of E-Cadherin
in lobular carcinomas of the breast.
Immunohistochemical staining on FNA cell block preparations showed positive staining for E-Cadherin
, CD10 (Figure 4), AMACR (Figure 5), and cytokeratin AE1/AE3.
4] Genes: E6, E6 transforming protein [human papillomavirus 18]; E2, E2 regulatory protein [human papillomavirus]; E7, E7 transforming protein [human papillomavirus]; TP53, tumor protein p53; IFNG, interferon, gamma; TMC6 (previously known as EVER1), transmembrane channel-like 6; TMC8 (previously known as EVER2), transmembrane channel-like 8; DAPK, death-associated protein kinase 1; CDH1, cadherin 1, type 1, E-cadherin
(epithelial); RASSF1, Ras association (RalGDS/AF-6) domain family member 1; CDKN2A, cyclin-dependent kinase inhibitor 2A; FHIT, fragile histidine triad; MGMT, O-6-methylguanine-DNA methyltransferase; RARB, retinoic acid receptor, beta.
Absence of E-cadherin
membranous staining is characteristic of lobular carcinomas, including PLC (Figure 2, D).
is lost, cells become 'rouge' - they can detach from their surrounding tissues, move effortlessly through the circulatory system, grow and attach at new sites," said Hari Koul, PhD, investigator at the CU Cancer Center and professor and director of Urology Research at the University of Colorado School of Medicine, the study's senior author.
Washington, April 3 ( ANI ): A University of Colorado Cancer Center study has described for the first time a switch that regulates the production of the protein E-Cadherin
, the loss of which is a prerequisite for prostate cancer metastasis.
The switch from E-cadherin
to N-cadherin is a well-known indicator of the epithelial-to-mesenchymal transition (EMT) occurring in bladder cancer.