Differential expression of sprouty genes in hepatocellular carcinoma

被引:31
作者
Sirivatanauksorn, Yongyut [2 ]
Sirivatanauksorn, Vorapan [1 ]
Srisawat, Chatchawan [1 ]
Khongmanee, Amnart [1 ]
Tongkham, Chalita [1 ]
机构
[1] Mahidol Univ, Dept Biochem, Fac Med, Siriraj Hosp, Bangkok 10700, Thailand
[2] Mahidol Univ, Hepatopancreatobiliary & Transplant Surg Unit, Div Gen Surg, Dept Surg,Fac Med,Siriraj Hosp, Bangkok 10700, Thailand
关键词
Sprouty; SPRY; hepatocellular carcinoma; cirrhosis; angiolymphatic invasion; HUMAN PROSTATE-CANCER; TUMOR-SUPPRESSOR; KINASE PATHWAY; GROWTH; INHIBITOR; PROTEINS; CELLS; OVEREXPRESSION; MIGRATION; SPRY1;
D O I
10.1002/jso.22095
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background and Objectives Sprouty (Spry) proteins are important modulators of the RTK/Ras/MAPK pathway, overactivation of which is associated with hepatocellular carcinoma (HCC). Thus far, the roles of Sprouty in HCC is still unclear. Methods: The expressions of SPRY1, SPRY2, SPRY3, and SPRY4, at the mRNA levels were determined by quantitative RT-PCR in paired HCC and non-tumor liver tissues from 31 patients. Results: The expression levels of SPRY1, SPRY2, and SPRY4 in tumor tissues were significantly different from those in non-tumor tissues with the average log fold change values of 0.15, -0.34, and -0.37, respectively; however, that of SPRY3 was not significantly different. SPRY1 expression was also found to be significantly up-regulated in the cases without underlying cirrhosis compared with those with cirrhosis (log fold change of 0.35 and -0.02, respectively, P < 0.05), whereas SPRY2 expression was significantly lower in the cases with advanced HCC (log fold change of -0.12 and -0.52 in early and advanced stages, respectively, P < 0.05) and in those with angiolymphatic invasion (log fold change of -0.47 and -0.16 in the presence and absence thereof, P < 0.05). Conclusion: This study demonstrates that Sprouty genes are differentially expressed in HCC and might provide some insight into their roles in HCC carcinogenesis. J. Surg. Oncol. 2012;105:273-276. (C) 2011 Wiley Periodicals, Inc.
引用
收藏
页码:273 / 276
页数:4
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