结肠癌中PTEN和HCCR-1的表达及临床意义

Expression and Prognostic Significance of PTEN and HCCR-1 in Colorectal Cancer

目的探讨PTEN与HCCR1在结肠癌组织中的表达及意义。方法应用免疫组织化学sP法检测66例结肠癌组织、30例正常结肠组织中PTEN和HCCR1的表达，分析HCCR1的表达与临床病理特征的关系。结果PTEN在30例正常结肠组织中28例阳性表达．表达率为93．4％；在66例结肠癌组织中14例为阳性表达，表达率为36％。HCCRI在30正常组织中无阳性表达，表达率为O％．在66结肠癌组织中有49例阳性表达，阳性率74．2％，其阳性表达与患者年龄、性别、肿瘤大小、肿瘤部位均无明显相关fP〉O05），与组织分化程度、有无淋巴结转移和Dukes分期相关（P〈0．05）。癌组织中PTEN与HCCR1的表迭呈负相关（F=-0．531，n=66，p=0．000）。结论结肠癌组织中HCCR-1处于过度表达状态与结肠癌的发生密切相关，PTEN作为抑癌基因在结肠癌的发生发展中发挥作用，PTEN可能通过P13K／Akt信号转导通路调节HCCR1的表达。

Objective To explore the expression of PTEN and HCCR-1 in colorectal carcinoma tissues as well as their clinical prognostic significance. Methods The expression of PTEN and HCCR-1 in 66 cases of colorectal carcinoma tissue and 30 cases of normal colorectal tissue around the loci were detected by SP immunohistochemistry. The expressions of HCCR-1 and correlations to the clinic pathological features and prognosis of colorectal carcinoma were analyzed. Results There were 28 cases of PTEN positive express in 30 cases of normal colonieal tissues, the positive rate of expression was 93.4%, there were 14 cases of PTEN positive express in 66 cases of colorectal carcinoma tissues, the positive rate of expression was 3.6%. There was no case of HCCR-1 positive express in 30 cases of normal colonical tissues, the positive rate of expression was 0%, there were 49 cases of PTEN positive express in 66 cases of colorectal carcinoma tissues, the positive rate of expression was 74.2%, the positive expression of HCCR-1 was related to differentiation grade, lymph node metastases, Dukes＂ stage （P〈0.05）. The positive expression of PTEN and HCCR-1 was negatively correlation in colorectal carcinoma tissues （r=--0.531, n=66, P=0.000）. Conclusion The HCCR-1 stand in over-expression status at the eoloreetal carcinoma tissues, HCCR-1 may play an important role in the occurrence of colorectal carcinoma. PTEN play a tumor suppressor gene role in the occurrence of eolorectal carcinoma, PTEN regulate the expression of HCCR-1 may be through the PI3K/Akt signal transduction pathway.