【摘要】：目的研究LKB1在肝細(xì)胞肝癌(hepatocellular carcinoma,HCC)上皮-間質(zhì)轉(zhuǎn)化(epithelial-mesenchymal transition,EMT)中的作用。研究方法收集鄭州大學(xué)人民醫(yī)院病例資料完整的HCC標(biāo)本90例、慢性乙肝肝硬化組織和肝血管瘤組織各30例。通過免疫組化的方法分別檢測HCC、乙肝肝硬化組織和肝血管瘤組織中LKB1和EMT相關(guān)分子E-cadherin、N-cadherin的表達(dá)。結(jié)果選取的90例HCC標(biāo)本中,LKB1陽性表達(dá)率為31.1%(28/90)。明顯低于其在乙肝肝硬化組織和肝血管瘤組織中的的表達(dá),陽性表達(dá)率分別為93.3%(28/30)和96.6%(29/30)。E-cadherin在乙肝肝硬化組織和肝血管瘤組織中的陽性表達(dá)率分別為73.3%(22/30)和66.6%(20/30),而HCC組織其陽性表達(dá)率為45.6%(41/90)。與之相反,N-cadherin在HCC組織中表現(xiàn)為表達(dá)增高(70.0%,63/90),乙肝肝硬化組織和肝血管瘤組織中表現(xiàn)為低表達(dá)(8/30,26.6%;4/30,13.3%)。LKB1在HCC中的表達(dá)與腫瘤直徑、腫瘤有無包膜、門靜脈受侵犯以及TNM分期有關(guān)(p0.05),而與年齡、性別、感染乙肝病毒無關(guān);腫瘤直徑、HCC包膜缺失、門靜脈侵犯與E-cadherin表達(dá)降低有關(guān)(p0.05)。腫瘤包膜、TNM分期、門靜脈侵犯與N-cadherin表達(dá)增高有關(guān)(p0.05)。LKB1在高分化和中分化HCC中的陽性表達(dá)率為(36.99%,27/73)高于其在低分化HCC中的陽性表達(dá)率(5.88%,1/17),存在統(tǒng)計(jì)學(xué)差異(p0.05)。LKB1在HCC中的表達(dá)與E-cadherin的表達(dá)呈正相關(guān),具有統(tǒng)計(jì)學(xué)差異(p0.05),LKB1在HCC中的表達(dá)與N-cadherin的表達(dá)呈負(fù)相關(guān),具有統(tǒng)計(jì)學(xué)差異(p0.05)。結(jié)論1.隨著HCC分化程度越低,LKB1的表達(dá)也隨之降低,HCC中LKB1的表達(dá)與分化程度相關(guān);2.LKB1、E-cadherin在HCC中表達(dá)降低,N-cadherin在HCC中表達(dá)增高,LKB1表達(dá)降低與HCC上皮-間質(zhì)轉(zhuǎn)化相關(guān)。
[Abstract]:Objective to study the role of LKB1 in epithelial-interstitial transformation (epithelial-mesenchymal transition,EMT) of hepatocellular carcinoma (hepatocellular carcinoma,HCC). Methods 90 HCC specimens were collected from Renmin Hospital of Zhengzhou University, 30 cases from liver cirrhosis and 30 cases from hemangioma of liver. The expression of LKB1 and EMT related molecules E-cadherin in liver cirrhosis and hemangioma tissues of HCC, hepatitis B were detected by immunohistochemical method. Results the positive rate of LKB1 in 90 HCC samples was 31. 1% (28 / 90). The positive expression rates of E-cadherin in liver cirrhosis and hemangioma were 93.3% (28 / 30) and 96.6% (29 / 30), respectively. The positive expression rates of E-cadherin in liver cirrhosis and hepatic hemangioma were 73.3% (2230 / 30) and 66.6% (2030), respectively. The positive rate of E-cadherin in HCC was 45.6% (41 / 90). In contrast, the expression of N-cadherin in HCC was increased (70.063 / 90), and the expression of LKB1 in liver cirrhosis and hemangioma was low (83026.6 / 4 / 3013.3%). The expression of LKB1 in HCC was correlated with the diameter of tumor, and the tumor had no capsule. Portal vein invasion and TNM staging were correlated with age, sex and hepatitis B virus infection (p0.05). The tumor diameter of HCC was absent and portal vein invasion was associated with decreased expression of E-cadherin (p0.05). TNM staging of tumor capsule The positive expression rate of LKB1 in well-differentiated and moderately differentiated HCC was higher than that in poorly differentiated HCC (p0.05). The expression of LKB1 in HCC was significantly higher than that in poorly differentiated HCC (5.8820 / 17). There was a positive correlation between the expression of LKB1 in HCC and the expression of E-cadherin. The expression of LKB1 in HCC was negatively correlated with the expression of N-cadherin (p0.05). Conclusion 1. With the lower the differentiation of HCC, the lower the expression of LKB1, the lower the expression of LKB1E-cadherin in HCC and the lower the expression of N-cadherin in HCC. The decrease of LKB1 expression was related to the epithelial-interstitial transformation of HCC.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R735.7

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