It has been suggested that inactivation of the cadherin-mediated cell-cell adhesion system plays a role in the initial steps of cancer invasion and metastasis. Expression of E-cadherin and its intracytoplasmic binding molecules, alpha-catenin, beta-catenin and plakoglobin was examined immunohistochemically in 96 esophageal squamous cell carcinomas to investigate the association between their expression and the prognosis for patients with esophageal cancer. Reduced E-cadherin, alpha-catenin, beta-catenin and plakoglobin expression was observed in 44, 72, 73 and 88% of the tumors, respectively. Reduced E-cadherin, alpha-catenin, beta-catenin and plakoglobin expression correlated closely with the differentiation grade of the esophageal squamous cell carcinoma (p < 0.05). Downregulation of alpha-catenin was associated with a poor prognosis in patients with esophageal squamous cell carcinoma (p < 0.05). This result suggests that downregulation of alpha-catenin, which may reflect dysfunction of the cadherin-mediated cell-cell adhesion system, is a factor indicating a poor prognosis in patients with esophageal cancer.

Adult↗

PubMedDate not supplied

Expression of basic fibroblast growth factor and its receptor by fibroblast, macrophages and mast cells in hypertrophic scar.

Basic fibroblast growth factor (bFGF) is a potent mitogenic and chemotactic factor for endothelial cells and fibroblasts. To investigate the pathological role of bFGF in hypertrophic scar, we performed an immunohistochemical study on bFGF and bFGF receptor (bFGF-R) in hypertrophic scar (HS) including keloid, in comparison with normal scar (non-HS) and normal skin. To identify bFGF and bFGF-R positive cells, double immunostaining with antibody to mast cell (MC, tryptase) or tissue macrophage (CD68) was carried out. The expression of bFGF and bFGF-R in cultured fibroblasts from scars was also examined. In HS, many positive cells for bFGF or bFGF-R were observed between collagen bundles in addition to the positive area in normal skin. Although most of the positive cells for bFGF or bFGF-R were fibroblasts, the positive rates of bFGF in macrophages was also increased (p < 0.005). The positive rate of bFGF in MCs and the positive rates of bFGF-R in macrophages and MCs were not changed. No obvious difference was observed between non-HS and normal skin in the expression of bFGF and bFGF-R. Cultured fibroblasts from HS showed a strong nuclear staining of bFGF, but not from non-HS and normal skin. bFGF-R was equally expressed with a diffuse cytoplasmic pattern by fibroblasts from all sources. bFGF may play an important role in the pathological fibrotic process of HS in which fibroblasts are persistently activated. Cellular source of the abnormal bFGF in HS may be both fibroblasts themselves and macrophages.

Adult↗

PubMedDate not supplied

Apoptosis of androgen-independent prostate cell line induced by inhibition of fatty acid synthesis.

Androgen-dependent prostate cancer cells eventually progress to androgen -independent cells after hormonal manipulation. Due to chemotherapeutic drug resistance and toxic side effects, new targets for antineoplastic therapy are urgently needed. In the present study, cerulenin, a fatty acid synthase inhibitor, was used to induce the death of androgen-independent prostate cancer cells. Cerulenin induces the apoptosis of TSU-prl cells based upon the temporal sequence of DNA fragmentation, morphologic changes and loss of cell viability. During apoptotic process induced by the agents, expression of cyclin-dependent kinase inhibitors p21 and p27 increased, whereas expression of cyclin D1 decreased. Flow cytometric analysis showed that the treatment resulted in a block in G2/M of the cell cycle. These results demonstrated that inhibition of fatty acid synthesis could be a target to treat hormone-independent prostate cancer cells via apoptosis, and cyclin-dependent kinase inhibitors played some role during apoptotic pathway.

Androgens↗