ABSTRACT: Hsp90? (heat shock protein 90?), one of the important molecular chaperones in cancer cell signal transduction, has been a new candidate target for cancer therapy. Cyclin B1, the client protein of Hsp90?, plays a key role as a mitotic cyclin in the G2-M phase transition during the cell cycle progression. However, the relationship between the level of HSP90? and cyclin B1, the location of Hsp90? and cyclin B1 in prognosis of esophageal squamous cell carcinoma (ESCC) has not been examined. Here, we demonstrate that the diagnostic significance of Hsp90? and cyclin B1 by immunohistochemistry and the association of Hsp90? and cyclin B1 expression in ESCC. In the specimens from 105 ESCC patients (81 stained with Hsp90? antibody by Immunohistochemistry, 65 with cyclin B1 antibody, and among them, 41 paired specimens were stained with Hsp90? and cyclin B1 respectively, and then checked for the correlation of the level and location of Hsp90? and cylcin B1. The positivity rate of Hsp90? and cyclin B1 expression were 96.3% (78 of 81) and 84.6% (55 of 65) respectively. Both of them, the expression levels are associated with the clinical pathological stage (Hsp90?, p=0.027; cyclin B1, p=0.007). No association was found between Hsp90? or cyclin B1 and gender, age, tumor location. As to TMN stage, there is no association with the level of Hsp90?, However, cyclin B1 expression is significantly related to tumor status (p=0.002). Interestingly, Hsp90? expression was negatively correlated to cyclin B1 expression (Gamma=-0.692, p=0.007) in the keratin pearls though there is a positive correlation in the other areas of tumor (Gamma=0.503, p=0.015), which suggest Hsp90? might play diverse roles in the cyclin B1 expression and cyclin B1 related cell cycle regulation in the different area of tumor. These findings demonstrated that the expression of Hsp90?, cyclin B1 protein is associated with tumor malignancy and prognosis for patients with human esophageal squamous cell carcinoma, and Hsp90? might be involved in cyclin B1 expression regulation and cell cycle regulation in keratin peal formation of ESCC.
