Sulkowska Urszula, Wincewicz Andrzej, Kanczuga-Koda Luiza, Koda Mariusz, Sulkowski Stanislaw
a Department of General Pathomorphology , Medical University of Bialystok , Bialystok , Poland.
b Department of Pathology (NZOZ Zakład Patologii Spółka z o.o.), Non-Public Health Care Unit , Kielce , Poland.
Gynecol Endocrinol. 2018 Feb;34(2):171-174. doi: 10.1080/09513590.2017.1379494. Epub 2017 Sep 22.
E-cadherin is a factor of good prognosis in endometrioid adenocarcinomas, while STAT3 is an oncogenic driver of carcinogenesis. E-cadherin, Bak, Bcl-xL and STAT3 were immunohistochemically detected in 78 human endometrioid adenocarcinomas. E-cadherin correlated with STAT3 (p <. 001, r = 0.537) as well as Bak (p = .005, r = 0.314) and Bcl-xL (p = .002, r = 0.340) in the whole study group. In G2 tumors, E-cadherin associated with Bak (p = .021, r = 0.319), Bcl-xL (p = .026, r = 0.309) and STAT3 (p <.001, r = 0.513) but not in G3 adenocarcinomas. E-cadherin correlated with Bak and Bcl-xL in both G1- and estrogen receptor (ER)-negative tumors with significant relation of E-cadherin and STAT3 in G1- and ER-negative tumors. Antigrowth synergy of expression was preserved for antiapoptotic Bak and proliferation-suppressing E-cadherin in IA adenocarcinomas (p = .031, r = 0.342) with no significance between Bak and E-cadherin or STAT3 and emerging correlation between E-cadherin and Bcl-xL in IB + II tumors instead (p = .003, r = 0.472). E-cadherin correlated with Bak and Bcl-xL in ER-positive adenocarcinomas (p = .002, r = 0.382 and p <.001, r = 0.439, respectively) but not in ER-negative tumors. In conclusion, expression deregulation of studied proteins is reflected in selective loss of correlation between suppressors of tumor growth (E-cadherin and Bak) presumably due to progressing impairment of growth-inhibitory properties of clone of neoplastic cells within higher staging and poorer differentiation.
E-钙黏蛋白是子宫内膜样腺癌预后良好的一个因素，而信号转导和转录激活因子3（STAT3）是致癌作用的致癌驱动因子。在78例人子宫内膜样腺癌中对E-钙黏蛋白、Bak、Bcl-xL和STAT3进行了免疫组织化学检测。在整个研究组中，E-钙黏蛋白与STAT3相关（p <.001，r = 0.537），也与Bak相关（p = 0.005，r = 0.314）和Bcl-xL相关（p = 0.002，r = 0.340）。在G2期肿瘤中，E-钙黏蛋白与Bak相关（p = 0.021，r = 0.319）、Bcl-xL相关（p = 0.026，r = 0.309）和STAT3相关（p <.001，r = 0.513），但在G3期腺癌中不相关。在G1期和雌激素受体（ER）阴性肿瘤中，E-钙黏蛋白与Bak和Bcl-xL相关，在G1期和ER阴性肿瘤中E-钙黏蛋白与STAT3有显著相关性。在IA期腺癌中，抗凋亡的Bak和抑制增殖的E-钙黏蛋白的表达具有抗生长协同作用（p = 0.031，r = 0.342），而在Bak与E-钙黏蛋白或STAT3之间无显著相关性，相反在IB + II期肿瘤中E-钙黏蛋白与Bcl-xL出现相关性（p = 0.003，r = 0.472）。在ER阳性腺癌中，E-钙黏蛋白与Bak和Bcl-xL相关（分别为p = 0.002，r = 0.382和p <.001，r = 0.439），但在ER阴性肿瘤中不相关。总之，所研究蛋白的表达失调表现为肿瘤生长抑制因子（E-钙黏蛋白和Bak）之间相关性的选择性丧失，这可能是由于在更高分期和更低分化的肿瘤细胞克隆中生长抑制特性的逐渐受损所致。
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