Negative E-∕P-cadherin and positive fibronectin immunophenotype may be associated with aggressive gastric carcinomas and supports the EMT involvement in gastric carcinogenesis.
Given the roles of fibronectin in risk stratification and in the frontline therapeutics of common carcinomas, such as renal cell cancer, we explored fibronectin immunoexpression status and its associations with clinicopathological variables and survival in a well-defined cohort of NPC patients.
Differences in both fibronectin and MUC1 expression between the follicular carcinomas and the follicular adenomas were also significant (P = .025 and .045, respectively).
Although up-regulation of FN has been noted in gene profiles of carcinomas compared with normal tissue, reduced FN expression has been described at the peripheral margins of invading tumors.
Molecular basis for the presence of glycosylated onco-foetal fibronectin in oral carcinomas: the production of glycosylated onco-foetal fibronectin by carcinoma cells.
Only 5 genes were overexpressed in all carcinomas including fibronectin 1 (FN1), tissue metalloproteinase inhibitor 1 (TIMP1), biglycan (BGN), tenascin-C (HXB), and insulin-like growth factor binding protein 5 (IGFBP5), whereas 16 genes were underexpressed.
Therefore, the much increased expression of oncofetal fibronectin mRNA in these carcinomas is not caused by the alternation in splicing, but may be caused by an increase in promoter activity or stability of mRNA of the fibronectin gene.
Initial results suggest a correlation between the amount of ED-B+ and de novo-glycosylated fibronectin in tumour stroma and the behaviour of carcinomas with regard to their invasiveness and propensity for metastatic dissemination.
These results demonstrate that accumulation of FN adjacent to oral carcinomas includes both the ED-B-containing isoform and the isoform derived by O-glycosylation.