Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P52742 (pT3)
 1,034 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

E-cadherin/beta-catenin complex has a critical role in cell-cell adhesion. beta-Catenin is a critical component of the highly conserved Wnt signaling pathway that regulates cell proliferation and differentiation. Wnt signaling leads to the stabilization of cytosolic beta-catenin and to translocation to the nucleus, where it binds with T-cell factor and promotes the transcription and changes in target gene expression, including matrix metalloproteinases. In this study, we analyzed paraffin-embedded specimens from 42 patients with pT3 rectosigmoid cancer for E-cadherin, beta-catenin, and matrix metalloproteinase-7(MMP-7, matrilysin) expression using immunohistochemistry. Seventy-four and 79% of tumors expressed beta-catenin and E-cadherin, respectively. Nuclear expression of beta-catenin was detected only in 26.1% of tumors. Forty-five percent of the rectosigmoid cancers showed strong expression of MMP-7. It was revealed that membranous or cytoplasmic beta-catenin expression was significantly related to E-cadherin and MMP-7 expression. No significant association was seen between E-cadherin, beta-catenin, or MMP-7 expression and some clinicopathologic features. Our results may contribute to the functional interaction between beta-catenin and MMP-7. Further studies on Wnt/beta-catenin and MMP-7 gene activity and protein expression are necessary to better understand the pathogenesis of colorectal carcinoma.
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PMID:E-cadherin, beta-catenin adhesion complex and relation to matrilysin expression in pT3 rectosigmoid cancers. 1867 69

E1AF is associated with malignant aggressiveness via regulation of matrix metalloproteinases (MMPs), which play pivotal roles in invasion through the degradation of extracellular matrix of tissues surrounding tumors. However, the clinical significance of E1AF and MMPs in patients with prostate cancer is not fully understood. We reviewed 50 tissue samples from patients with T2-3N0M0 prostate cancer who had undergone radical operation. Expression levels of E1AF, MMP-1, -3, -7, -9 and -14 were determined semiquantitatively by immunohistochemistry. The mean +/- SD percentage of E1AF-stained cancer cells was 8.56 +/- 5.22, and it was significantly higher (p < 0.001) than the E1AF-immunostaining index of normal cells (1.17 +/- 0.61). E1AF immunostaining index in pT3 (12.74 +/- 4.80) was significantly higher (p < 0.001) than that in pT2 (5.78 +/- 3.31). Although E1AF expression correlated with that of MMP-7 and MMP-9 (r = 0.47, p < 0.001 and r = 0.41, p = 0.004, respectively), multivariate analysis showed that E1AF correlated with only MMP-7 expression (OR = 5.81, 95% CI = 1.27-26.59, p = 0.023). Our results demonstrated that increased expression of E1AF is involved in tumor aggression of prostate cancer. This finding may be influenced by regulation of MMP-7. We speculate that E1AF is a possible target in treatment and prevention of tumor growth in prostate cancer.
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PMID:E1AF expression is associated with extra-prostatic growth and matrix metalloproteinase-7 expression in prostate cancer. 1984 29