Differential expression of galectin-3, β-catenin, and cyclin D1 in adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma of salivary glands
Differential expression of galectin-3, β-catenin, and cyclin D1 in adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma of salivary glands
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DOI：
10.1111/j.1600-0714.2009.00776.x
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发表时间：
2009-10-01
影响因子：
3.3
通讯作者：
de Sousa, S. O. M.
中科院分区：
文献类型：
--
作者：
Ferrazzo, K. L.;Neto, M. M.;de Sousa, S. O. M.
背景：Galectin-3与甲状腺、前列腺癌和唾液腺肿瘤等恶性肿瘤的进展有关。最近，有研究表明，该蛋白可能是β-连环蛋白/Wnt途径的重要介体。此外，核Galectin-3的表达与细胞增殖有关，促进了细胞周期蛋白D1的激活。因此，本研究旨在探讨Galectin-3在腺样囊性癌(ACC)和多形性低级腺癌(PLGA)中的表达及其与β-catenin和Cyclin D1表达的相关性。方法：从圣保罗大学口腔外科病理中心收集15例福尔马林固定的石蜡包埋病例，用免疫组织化学方法分析Galectin-3蛋白的表达。结果：腺样囊性癌Galectin-3免疫染色主要分布在细胞核，而PLGA对Galectin-3的阳性反应主要是胞浆反应。在大多数病例中，两种肿瘤都表现出强烈的胞浆/核β-连环蛋白染色。15例PLGA中14例未检测到细胞周期蛋白D1的表达，10/15例ACC中5%以上的肿瘤细胞呈特异性核染色。在ACC中，细胞周期蛋白D1的表达与胞浆及胞核中Galectin-3的表达呈正相关(P<；0.05)。结论：在ACC中，Galectin-3可能通过激活细胞周期蛋白D1而参与细胞增殖。此外，Galectin-3在ACC中的核表达可能与该病变的更具侵袭性有关。尽管β-连环蛋白似乎在这两个病变的致癌过程中发挥了作用，但它似乎不能与Galectin-3结合来刺激细胞周期蛋白D1。
Background:Galectin-3 has been implicated in tumor progression of some malignancies as thyroid, prostate, and salivary gland tumors. Recently, it has been suggested that this protein may be an important mediator of the beta-catenin/Wnt pathway. Moreover, nuclear galectin-3 expression has been implicated in cell proliferation, promoting cyclin D1 activation. Thus, the present study aimed to correlate galectin-3 expression with beta-catenin and cyclin D1 expressions in adenoid cystic carcinoma (ACC) and in polymorphous low-grade adenocarcinoma (PLGA).Methods:Fifteen formalin-fixed paraffin-embedded cases of each tumor were retrieved from the files of the Surgical Oral Pathology Service at the University of Sao Paulo and the proteins were analyzed by immunohistochemistry.Results:Adenoid cystic carcinoma showed galectin-3 immunostaining mainly in the nuclei, while PLGA revealed a positive mostly cytoplasmic reaction to galectin-3 in the largest part of tumor cells. Both tumors showed intense cytoplasmic/nuclear staining for beta-catenin in majority of cases. Cyclin D1 immunoreactivity was not detected in 14/15 PLGA and showed specific nuclear staining in 10/15 cases of ACC in more than 5% of the neoplastic cells. Cyclin D1 expression was correlated with cytoplasmic and nuclear galectin-3 expression in ACC (P < 0.05).Conclusions:These results suggest that in ACC galectin-3 may play a role in cellular proliferation through cyclin D1 activation. In addition, nuclear expression of galectin-3 in ACC may be related to a more aggressive behavior of this lesion. Although beta-catenin seems to play a role in carcinogenesis in both lesions, it seems that it does not bind to galectin-3 for cyclin D1 stimulation.