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   <subfield code="a">Overexpression of SYF2 correlates with enhanced cell growth and poor prognosis in human hepatocellular carcinoma</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Shusen Zhang, Weidong Shi, Yuyan Chen, Zhiwei Xu, Jia Zhu, Tingting Zhang, Wei Huang, Runzhou Ni, Cuihua Lu, Xiubing Zhang]</subfield>
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   <subfield code="a">SYF2, also known as p29/NTC31/CBPIN, encodes a nuclear protein that interacts with Cyclin D-type binding-protein 1. SYF2has been reported to be involved in pre-mRNA splicing and cell cycle regulation. In the present study, we observed that SYF2 was obviously upregulated in HCC tumor tissues and cell lines, and its level was positively correlated with the tumor grade and Ki-67 expression, as well as poor prognosis of HCC. In vitro, using serum starvation-refeeding experiment, our results suggested that SYF2 was upregulated in proliferating HCC cells, and was positive correlated with the expression of PCNA and Cyclin D1. In addition, depletion of SYF2 decreased PCNA and Cyclin D1 levels. Accordingly, interference of SYF2 resulted in cells cycle arrest at G1/S phase in Huh7 HCC cells. Furthermore, we found that SYF2 might interact with Cyclin D1 and could confer doxorubicin resistance in HCC cells. These findings revealed that SYF2 might play a regulatory role in the proliferation of HCC cells. In summary, SYF2 may be a novel prognostic marker and serve as a potential therapeutic target in HCC.</subfield>
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