Guo Jun-Hui, Xing Guo-Lan, Fang Xin-Hui, Wu Hui-Fang, Zhang Bo, Yu Jin-Zhong, Fan Zong-Min, Wang Li-Dong
Jun-Hui Guo, Henan Province Hospital of TCM, Zhengzhou 450000, Henan Province, China.
World J Gastroenterol. 2017 Feb 28;23(8):1434-1442. doi: 10.3748/wjg.v23.i8.1434.
To understand the molecular mechanism of esophageal cancer development and provide molecular markers for screening high-risk populations and early diagnosis.
Two-dimensional electrophoresis combined with mass spectrometry were adopted to screen differentially expressed proteins in nine cases of fetal esophageal epithelium, eight cases of esophageal cancer, and eight cases of tumor-adjacent normal esophageal epithelium collected from fetuses of different gestational age, or esophageal cancer patients from a high-risk area of esophageal cancer in China. Immunohistochemistry (avidin-biotin-horseradish peroxidase complex method) was used to detect the expression of peroxiredoxin (PRX)6 in 91 cases of esophageal cancer, tumor-adjacent normal esophageal tissue, basal cell hyperplasia, dysplasia, and carcinoma , as well as 65 cases of esophageal epithelium from fetuses at a gestational age of 3-9 mo.
After peptide mass fingerprint analysis and search of protein databases, 21 differential proteins were identified; some of which represent a protein isoform. Varying degrees of expression of PRX6 protein, which was localized mainly in the cytoplasm, were detected in adult and fetal normal esophageal tissues, precancerous lesions, and esophageal cancer. With the progression of esophageal lesions, PRX6 protein expression showed a declining trend ( < 0.05). In fetal epithelium from fetuses at gestational age 3-6 mo, PRX6 protein expression showed a declining trend with age ( < 0.05). PRX6 protein expression was significantly higher in well-differentiated esophageal cancer tissues than in poorly differentiated esophageal cancer tissues ( < 0.05).
Development and progression of esophageal cancer result from interactions of genetic changes (accumulation or superposition). PRX6 protein is associated with fetal esophageal development and cancer differentiation.
了解食管癌发生发展的分子机制，为高危人群筛查及早期诊断提供分子标志物。
采用二维电泳结合质谱技术，对收集自不同孕周胎儿或中国食管癌高发区食管癌患者的9例胎儿食管上皮、8例食管癌及8例癌旁正常食管上皮中的差异表达蛋白进行筛选。采用免疫组织化学法（抗生物素蛋白-生物素-辣根过氧化物酶复合物法）检测91例食管癌、癌旁正常食管组织、基底细胞增生、发育异常及癌组织，以及65例孕龄3-9个月胎儿食管上皮中过氧化物酶（PRX）6的表达。
经肽质量指纹图谱分析及蛋白质数据库检索，鉴定出21种差异蛋白；其中部分为蛋白质异构体。在成人及胎儿正常食管组织、癌前病变及食管癌组织中均检测到PRX6蛋白不同程度的表达，其主要定位于细胞质。随着食管病变进展，PRX6蛋白表达呈下降趋势（P<0.05）。在孕龄3-6个月胎儿的食管上皮中，PRX6蛋白表达随年龄增长呈下降趋势（P<0.05）。高分化食管癌组织中PRX6蛋白表达明显高于低分化食管癌组织（P<0.05）。
食管癌的发生发展是基因改变（积累或叠加）相互作用的结果。PRX6蛋白与胎儿食管发育及癌分化相关。
