Shh、Gli1和p-Akt在食管癌中的表达及临床意义

Expressions of Shh,Gli1 and p-Akt in esophageal squamous cell carcinoma and their clinical significance

目的观测SHh信号通路关键冈子Shh、Gli1和PI3K/Akt信号通路的关键因子p-Akt在食管鳞状细胞癌(ESCC)中的表达情况,探讨上述因子的表达与ESCC各临床病理特征的关系和意义。方法采用免疫组织化学EnVision法检测108例手术治疗的ESCC组织及相应的癌旁正常食管黏膜标本Shh、Gli1和p-Akt的表达情况。结果在108例ESCC组织中Shh、Gli1和p-Akt的阳性表达率分别为70.1%(76/108)、76.9%(83/108)和65.7%(71/108)108例癌旁正常食管黏膜中Shh、Gli1和p-Akt的阳性表达率分别为13.9%(15/108)、13%(14/108)和15.7%(17/108)。ESCC组织中Shh、Gli1和p-Akt的阳性表达率显著高于相应的癌旁正常食管黏膜的表达(P<0.05);Shh、Gli1和p-Akt表达与肿瘤是否有淋巴结转移密切相关(P<0.05),ESCC中Shh的表达与Gli1的表达成正相关(r1=0.750,P<0.01),Gli1表达与p-Akt表达呈正相关(r2=0.621,P<0.01)。结论 ESCC中SHh通路和PI3K/Akt通路是普遍激活的,Gli1与p-Akt可作为预测转移潜能和预后状况的有价值的指标,联合抑制SHh通路和PI3K/Akt通路对于治疗食管癌可能更有效。

Objective To observe the expression of Shh, Glil and p-Akt in human esophageal squamous cell carcinoma （ESCC） , and study the relationship between the expression amt the clinieopathoh）gieal data. Methods Tissue specimens were collected dur- ing thoracic surgery from 108 patients and were divided into twogroups：ESCC tissue gronp and adjacent normal esophageal tissue- group. The expressions of Shh, Gill and p-Akt were detected by irnmunohistoehemical staining. Results hnmunochemistry showed in 108 ESCC tissue slices, the positive rates of Shh, Glil and p-Aktwere 70.1% （76/108） , 76.9% （83/108） and 65.7% （71/108） , respectively, whereas in the adjacent normal esophageal mueosa, that of Shh, （;lil and p-Akt were 13.9% （15/ 108） ,13.0% （14/108） and 15.7% （17/108）. The expressions ofShh, Clil and p-AM were higher in ESCC than in the adja- cent normal esophageal mucosa （P 〈 0.05 ）. The expressions of Shh, Glil and p-Akt were significantly correlated with lymph node metastasis（ P 〈 0.05 ）. Statistical analysis showed that the expression of Shh was positive associate with Glil in ESCC（ rl = 0. 750, P 〈 0.01 ） , whereas that of Glil was positive associate with p-Aktin ESCC （ r2 = 0. 621, P 〈 0.01 ）. Conclusion The expressions of Shh, Glil and p-Akt are elevated in ESCC, which indicates that Shh and PI3K/Akt pathways are usually activated in most ESCC. Joint inhibition of these pathways may be more effective in thetreatmcnt strategy of ESCC.