Department of Biochemistry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.
Cancer Invest. 2011 Jan;29(1):42-8. doi: 10.3109/07357907.2010.512597. Epub 2010 Sep 27.
Proteins do not operate as individual units, and components of intracellular canonical pathways often cross talk in tumor genesis. We hypothesized that G-protein-coupled receptor 56 (GPR56), transglutaminase (TG2), and nuclear factor-κB (NF-κB) may collaborate in interconnected pathways and contribute to the aggressive behavior of esophageal squamous cell carcinoma (ESCC). Immunohistochemical analysis of GPR56, TG2, and NF-κB was carried out using ESCC tissue microarrays. Immunostaining of all the three proteins revealed a significant increase in their expression in ESCCs as compared with normal epithelia and correlated with their concomitant expression. A significant correlation between GPR56, TG2, and NF-κB was observed that correlated with nodal metastasis and tumor invasion in ESCCs.
蛋白质并非作为独立单元发挥作用,细胞内经典途径的组成部分在肿瘤发生中经常相互交流。我们假设 G 蛋白偶联受体 56(GPR56)、转谷氨酰胺酶(TG2)和核因子-κB(NF-κB)可能在相互关联的途径中协作,并有助于食管鳞状细胞癌(ESCC)的侵袭行为。使用 ESCC 组织微阵列进行 GPR56、TG2 和 NF-κB 的免疫组织化学分析。与正常上皮相比,所有三种蛋白质的免疫染色在 ESCC 中均显示出表达显著增加,并与它们的共表达相关。在 ESCC 中观察到 GPR56、TG2 和 NF-κB 之间存在显著相关性,与淋巴结转移和肿瘤浸润相关。