Bai Peng, Xiao Xue, Zou Juan, Cui Lin, Bui Nguyen Tri M, Liu Jinsong, Xiao Jianguo, Chang Bin, Wu Jin, Wang He
West China School of Preclinical and Forensic Medicine;
Exp Ther Med. 2012 Jun;3(6):1026-1032. doi: 10.3892/etm.2012.523. Epub 2012 Mar 22.
Esophageal carcinoma is the sixth most common cause of cancer-related mortality in the world. Senescence and apoptosis are assumed to be two main mechanisms that inhibit age-related carcinogenesis. p14(ARF), p15(INK4b) and p16(INK4a), which are known to induce senescence by regulating G(1) cell cycle arrest, have been identified as senescence markers. However, the mechanism by which senescence and apoptosis causes neoplasia in esophageal squamous cell carcinoma (ESCC) has not been identified. In this study, 20 cases of normal esophageal tissues, 11 cases of esophageal intraepithelial dysplasia (EID) and 60 cases of ESCC were obtained and pathologically diagnosed. Immunohistochemical staining was performed to assess the expression of p14(ARF), p15(INK4b), p16(INK4a), skp2, bcl-2 and ki-67. The senescence markers p14(ARF) and p16(INK4a) were found to be expressed in 15 and 10% of the normal tissues, 82 and 73% of the EID cases and 100 and 88% of the ESCC cases, respectively. The expression of p15(INK4b) was low in normal tissues, while 92% of the ESCC specimens were diffusely and markedly stained, involving the basal, middle and upper portion of the epithelium. The nuclear expression markers ki-67 and skp2 were highly expressed in ESCC tissues (100 and 72%, respectively). bcl-2 was expressed weakly in normal tissues (10%) and demonstrated various staining patterns in carcinoma specimens (strong in 60%, negative in 40%). MI was 0.09% in normal tissues and 0.95% in the ESCC specimens. Apart from the increased proliferation in esophageal carcinogenesis, as indicated in the ki-67 and skp2 indices, there was an increased expression of senescence-associated molecular markers in the ESCC specimens, which indicates that the senescence pathway may be activated and become a part of cancer development. Of greatest interest to us was that, when compared with clinical information, the expression of the senescence markers was markedly high in the poorly differentiated specimens with lymph node metastasis, indicating that senescence markers may have diagnostic potential in clinical settings.
食管癌是全球第六大常见的癌症相关死亡原因。衰老和凋亡被认为是抑制与年龄相关的致癌作用的两个主要机制。已知通过调节G(1)期细胞周期停滞来诱导衰老的p14(ARF)、p15(INK4b)和p16(INK4a)已被确定为衰老标志物。然而,衰老和凋亡导致食管鳞状细胞癌(ESCC)发生肿瘤形成的机制尚未明确。在本研究中,获取了20例正常食管组织、11例食管上皮内瘤变(EID)和60例ESCC病例,并进行了病理诊断。进行免疫组织化学染色以评估p14(ARF)、p15(INK4b)、p16(INK4a)、skp2、bcl-2和ki-67的表达。发现衰老标志物p14(ARF)和p16(INK4a)在正常组织中的表达率分别为15%和10%,在EID病例中的表达率分别为82%和73%,在ESCC病例中的表达率分别为100%和88%。p15(INK4b)在正常组织中表达较低,而92%的ESCC标本呈弥漫性强染色,累及上皮的基底、中层和上层部分。核表达标志物ki-67和skp2在ESCC组织中高表达(分别为100%和72%)。bcl-2在正常组织中弱表达(10%),在癌标本中表现出多种染色模式(60%为强阳性,40%为阴性)。正常组织中的有丝分裂指数(MI)为0.09%,ESCC标本中的MI为0.95%。除了ki-67和skp2指数所示的食管癌变过程中增殖增加外,ESCC标本中衰老相关分子标志物的表达也增加,这表明衰老途径可能被激活并成为癌症发展的一部分。我们最感兴趣的是,与临床信息相比,衰老标志物在伴有淋巴结转移的低分化标本中的表达明显较高,这表明衰老标志物在临床环境中可能具有诊断潜力。