Wang Zhihui, Tropè Claes G, Suo Zhenhe, Trøen Gunhild, Yang Guanrui, Nesland Jahn M, Holm Ruth
Division of Pathology, The Norwegian Radium Hospital, Rikshospitalet University Hospital, Oslo, Norway.
BMC Cancer. 2008 Oct 24;8:308. doi: 10.1186/1471-2407-8-308.
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.
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.
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.
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.
14-3-3σ通过将细胞周期蛋白B1-CDC2复合物隔离在细胞质中促进G2/M期细胞周期停滞。14-3-3σ的下调在多种癌症中均有报道,可能与恶性转化有关。然而,14-3-3σ在外阴癌发病机制中的确切作用尚未完全明确,其蛋白表达对预后的影响也尚不清楚。
我们采用免疫组织化学方法研究了302例外阴鳞状细胞癌中14-3-3σ的表达情况,并分析其与临床病理因素及临床结局的关系。
在外阴癌的细胞质、细胞核及细胞质/细胞核中,14-3-3σ蛋白高表达分别见于72%、59%和75%的病例,低表达分别见于28%、41%和25%的病例。细胞质、细胞核及细胞质/细胞核中14-3-3σ的高表达与肿瘤直径较大显著相关(分别为p = 0.001、p = 0.002和p = 0.001),与深层浸润也显著相关(分别为p = 0.01、p = 0.001和p = 0.007)。14-3-3σ蛋白表达的变化与疾病特异性生存率无关。
我们的结果表明,14-3-3σ可能通过下调14-3-3σ蛋白参与了一部分外阴鳞状细胞癌的发生发展。14-3-3σ在细胞质和细胞核中的表达水平均与预后无关。