Expression of Livin and Caspase-3 in Colorectal Adenoma-Carcinoma Sequence and Their Correlation_West China Medical Journal

Authors：

WANG Yong ¹ , SONG Yicai ¹ , YIN Zuowen ¹ , YU Jun ¹ , LIU Junhui ¹ , LI Yifan ² , GUO MeiMei ³

1.Department of Gastrointestinal Surgery, 2. Central Laboratory, 3. Department of Digestion Medicine, Xiehe-Shenzhen Hospital, Huazhong University of Science and Technology, Shenzhen, Guangdong 518052, P. R. China;

Corresponding author：

Keywords：

Livin; Caspase-3; 结直肠腺瘤; 结直肠癌

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【摘要】　目的　探讨凋亡抑制蛋白Livin与凋亡蛋白Caspase-3在结直肠腺瘤-癌序列中的表达变化及其相关性。　方法　 2006年7月—2009年12月，采用免疫组织化学染色链霉菌抗生物素蛋白-过氧化物酶链接法streptavidin-peroxidese，SP）法检测18例正常黏膜、84例结直肠腺瘤、72例结直肠癌中Livin及Caspase-3的表达情况。　结果　结直肠腺瘤组织中Livin蛋白的阳性表达率明显高于正常黏膜组织（P lt;0.05），而低于腺癌组（P lt;0.05）；腺瘤组内绒毛状腺瘤与管状腺瘤相比较，Livin蛋白表达率差异有统计学意义（P lt;0.05）。结直肠腺瘤组织中Caspase-3的阳性表达率明显高于正常黏膜组织（P lt;0.05）；而腺瘤组织与癌组织之间Caspase-3阳性表达率差异（P lt;0.05）；腺瘤组内绒毛状腺瘤与管状腺瘤相比较，Caspase-3蛋白阳性表达率差异无统计学意义（P gt;0.05）。Livin表达与Caspase-3表达呈负相关（P lt;0.05）。　结论　凋亡抑制蛋白Livin参与了大肠肿瘤的发生，且在大肠腺瘤-腺癌阶段起到了重要作用；凋亡抑制蛋白Livin与Caspase-3表达呈负相关，抑制Caspase-3蛋白的活性可能是Livin促进结肠癌发生的途径之一。
【Abstract】　Objective　 To investigate the expression of Livin and Caspase-3 among colorectal adenoma-carcinoma sequence, and to identify the relationship between Livin and Caspase-3 expression in colorectal adenoma-carcinoma sequence.　Methods　 Formalin-fixed paraffin embedded colorectal tissues from 174 patients, including 84 adenomas, 72 carcinomas, and 18 normal mucosa, were examined for expression of Livin and Caspase-3 by streptavidin-peroxidase (SP) immunohistochemistry between July 2006 and December 2009.　Results　 The positive rates of Livin protein expression in colorectal adenoma was significantly higher than that in normal mucosa (P lt;0.05), but lower than that in adenocarcinoma (P lt;0.05); the expression of Livin in tubular adenoma was significantly higher than that in villous adenoma (P lt;0.05). The positive rates of Caspase-3 protein expression in colorectal adenoma were significantly higher than that in normal mucosa and carcinoma (P lt;0.05), and the difference in positive rate of Caspase-3 expression was not significant between the villous adenoma and tubular adenoma (P gt;0.05). Livin expression had negative correlation with the Caspase-3 expression (P gt;0.05).　Conclusion　 The difference in expression of Livin between adenoma and adenocarcinoma indicates the potential value of it in carcinogenesis of colorectal cancer, which suggestes that suppressing Caspase-3 protein activity is one of the channels by which livin promotes colorectal carcinogenesis.

Citation： WANG Yong,SONG Yicai,YIN Zuowen,YU Jun,LIU Junhui,LI Yifan,GUO MeiMei. Expression of Livin and Caspase-3 in Colorectal Adenoma-Carcinoma Sequence and Their Correlation. West China Medical Journal, 2011, 26(6): 878-881. doi: Copy

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14.	石亮, 陈晓东, 林向阳. 细胞凋亡抑制蛋白研究进展 [J]. 国际检验医学杂志, 2007, 28(2): 153-157.

1. 　Jemal A, Siegel R, Ward E, et al. Cancer statistics[J]. CA Cancer J Clin, 2007, 57(1): 43-66.
2. 　Tannapfel A, Neid M, Aust D, et al. The origins of colorectal carcinoma: specific nomenclature for different pathways and precursor lesions[J]. Dtsch Arztebl Int, 2010, 107(43): 760-766.
3. 　Hiroshi K, Masao T, Hisashi S, et al. Expression of survivin correlates with apoptosis, proliferation, and angiogenesis during human colorectal tumorigenesis[J]. Cancer, 2001, 91(11): 2026-2032.
4. 　Huerta S, Goulet EJ, Livingston EH. Colon cancer and apoptosis[J]. Am J Surg, 2006, 191(4): 517-526.
5. 　Rupnarain C, Dlamini Z, Naicker S, et al. Colon cancer: genomics and apoptotic events[J]. Biol Chem, 2004, 385(6): 449-464.
6. 　Watson AJM. An overview of apoptosis and the prevention of colorectal cancer[J]. Crit Rev Oncolo/Hematolo, 2006, 57(2): 107-121.
7. 　Lin JH, Deng G, Huang Q, et al. KIAP, a novel member of the inhibitor of apoptosis protein family [J]. Biochem Biophys Res Commun, 2000, 279(3): 820-831.
8. 　Kasof GM, Gomes BC. Livin, a novel inhibitor of apoptosis protein family member [J]. J Biol Chem, 2001, 276(5): 3238-3246.
9. 　Vucic D, Stennicke HR, Pisabarro MT, et al. ML-IAP, a novel inhibitor of apoptosis that is preferentially expressed in human melanomas [J]. Curr Biol, 2000, 10(21): 1359-1366.
10. 　Crnkovic-Mertens I, Hoppe-Seyler F, Butz K. Induction of apoptosis in tumor cells by siRNA-mediated silencing of the livin/ML-IAP/KIAP gene [J]. Oncogene, 2003, 22(51): 8330-8336.
11. 　Liu B, Han M, Wen JK, et al. Livin/ML-IAP as a new target for cancer treatment [J]. Cancer Letter, 2007, 250(2): 168-176.
12. 　Vucic D, Frankin MC, Walweber HJ, et al. Engineering ML-IA P to produce an extraordinarily potent Caspase 9 inhibitor: implications for Smac-dependent anti-apoptotic activity of ML-IA P [J]. Biochem J, 2005, 385(1): 11-20.
13. 　Nachmias B, Ashhab Y, Bucholtz V, et al. Caspase-mediated cleavage converts Livin from an antiapoptotic to a proapoptotic factor implication for drug-resistant melanoma [J]. Cancer Res, 2003, 63(10): 6340-6349.
14. 　石亮, 陈晓东, 林向阳. 细胞凋亡抑制蛋白研究进展 [J]. 国际检验医学杂志, 2007, 28(2): 153-157.

West China Medical Journal

Expression of Livin and Caspase-3 in Colorectal Adenoma-Carcinoma Sequence and Their Correlation

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