Abstract
BACKGROUND: 14-3-3 sigma promotes G2/M cell cycle arrest by sequestering cyclin B1-CDC2 complex in cytoplasm. Down-regulation of 14-3-3sigma, which has been demonstrated in various carcinomas, may contribute to malignant transformation. However, the exact role of 14-3-3sigma in the pathogenesis of vulvar carcinoma is not fully characterized, and the prognostic impact of 14-3-3sigma protein expression is still unknown. METHODS: We investigated the 14-3-3sigma expression in a series of 302 vulvar squamous cell carcinomas using immunohistochemistry and its associations with clinicopathological factors and clinical outcome. RESULTS: In cytoplasm, nucleus and cytoplasm/nucleus of vulvar carcinomas high 14-3-3sigma protein expression was found in 72%, 59% and 75% of the carcinomas, respectively, and low levels in 28%, 41% and 25% of the cases, respectively. High level of 14-3-3sigma in cytoplasm, nucleus and cytoplasm/nucleus was significantly correlated to large tumor diameter (p = 0.001, p = 0.002 and p = 0.001, respectively) and deep invasion (p = 0.01, p = 0.001 and p = 0.007, respectively). Variations of 14-3-3sigma protein expression were not associated to disease-specific survival. CONCLUSION: Our results indicate that 14-3-3sigma may be involved in the development of a subset of vulvar squamous cell carcinomas by down-regulation of 14-3-3sigma protein. Neither cytoplasmic nor nuclear level of 14-3-3sigma expression was associated with prognosis.