SIN1 promotes invasion and metastasis of hepatocellular carcinoma by facilitating epithelial‐mesenchymal transition. Issue 12 (5th April 2013)

• Record Type: Journal Article
• Authors: Xu, Jiangfeng; Li, Xuedong; Yang, Hao; Chang, RuiMin; Kong, Chenchen; Yang, Lianyue
• Is Part Of: Cancer. Volume 119:Issue 12(2013)
• Page Start: 2247
• Page End: 2257
• Publication Date: 2013-04-05
• Subjects: Cancer -- Periodicals; Cancer -- Cytopathology -- Periodicals; 616.99405
• DOI: 10.1002/cncr.28023
• Languages: English
• ISSNs: 0008-543X

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="cncr28023-sec-0001" sec-type="section"> <title>BACKGROUND</title> <p>Stress‐activated protein kinase (SAPK) interacting protein 1 (SIN1) is essential for early embryonic development and is the key regulator of Akt, which plays an important role in various pathological conditions such as cancer. However, the biological function and clinical significance of SIN1 in hepatocellular carcinoma (HCC) remains unknown.</p> </sec> <sec id="cncr28023-sec-0002" sec-type="section"> <title>METHODS</title> <p>Real‐time quantitative reverse‐transcriptase polymerase chain reaction analysis, western blot analysis, and immunohistochemical staining were used to test the expression level of SIN1, and its correlation with clinicopathologic parameters as well as the prognosis for patients with HCC were analyzed. In addition, the biological function and molecular mechanisms of SIN1 in HCC were investigated.</p> </sec> <sec id="cncr28023-sec-0003" sec-type="section"> <title>RESULTS</title> <p>SIN1 levels were elevated predominantly in HCC tissues, and its level in solitary large HCC was significantly lower than those in nodular HCC (<italic>P</italic> = .016), but showed no significant differences between solitary large HCC and small HCC (<italic>P</italic> > .05). Levels of SIN1 were up‐regulated in highly metastatic HCC cell lines (HCCLM3 and MHCC97‐H), whereas their invasion and migration significantly decreased after depletion of SIN1. High expression of SIN1 was associated with tumor number (<italic>P</italic> = .012), capsular formation (<italic>P</italic> = .037), and venous invasion (<italic>P</italic> = .023) and was an independent risk factor for overall survival (<italic>P</italic> = .046). Finally, SIN1 was capable of promoting invasion and metastasis of HCC by facilitating epithelial‐mesenchymal transition.</p> </sec> <sec id="cncr28023-sec-0004" sec-type="section"> <title>CONCLUSIONS</title> <p>The current findings suggest that SIN1 plays an important role in HCC invasion and metastasis by facilitating epithelial‐mesenchymal transition. Cancer 2013;119:2247–2257. © 2013 American Cancer Society.</p> </sec> </abstract>