Objective To detect the expression of KiSS-1, KiSS-1R and MMP-9 in hepatocellular carcinoma (HCC). To study the correlation of KiSS-1, KiSS-1R and MMP-9 expression with invasion and metastasis of HCC, and to explore the underlying mechanisms. Methods The expression of KiSS-1 , KiSS-1R mRNA in 33 HCC samples, 26 non-neoplastic adjacent liver tissue samples and 13 non-neoplastic distant liver tissue samples were detected by RT-PCR. Tissue chips were constructed by modified manual tools, which contained HCC, non-neoplastic adjacent liver tissues, non-neoplastic distant liver tissues, normal liver tissues and intrahepatic metastasis lesions. The expression of KiSS-1 and MMP-9 protein was determined by tissue chips, immunohistochemistry and semi-quantitative image analysis in 150 HCC, 137 non-neoplastic adjacent liver tissue, 98 non-neoplastic distant liver tissues, 16 normal liver tissues and 37 intrahepatic metastasis lesion samples. Results The results of RT-PCR showed that compared with the non-neoplastic adjacent liver tissues and the non-neoplastic distant liver tissues, the expression of KiSS-1 mRNA in HCC was significantly lower (P＜0.01). The expression of KiSS-1R mRNA did not changed in HCC and non-neoplastic liver tissues (P＞0.05). The expression of KiSS-1 protein was lower in HCC with metastasis and in clinical stage Ⅲ than that in those with non-metastasis, and in clinical stages Ⅰ and Ⅱ . It was also higher in the primary than in the metastasis lesions (P＜0.01, respectively). The expression of MMP-9 was higher in tumors having peplos invasion and metastasis than in those with negative peplos invasion and non-metastasis. It was lower in the primary than the metastasis lesions (P＜0. 01, respectively).Negative correlation between KiSS-1 and MMP-9 expression was found in HCC(r=- 0.340,P＜0.01). Conclusions The imbalance between KiSS-1 and MMP-9 expression might play an important role in enhancing the invasive and metastatic capacity of HCC. Loss of KiSS-1 expression might predict an aggressive clinical behavior and was associated with metastatic potential in HCC.

Objective To identify and verify proteins that interact and collaborate with ATF3 in inhibiting hepatocarcinogenesis.Methods Immunoprecipitation (IP),co-IP and protein spectrum analysis were used to identify the protein which interacted with ATF3 in HepG2.Immunohistochemistry (IHC) and Western blot (WB) were used to detect the expression pattern of ATF3 and its candidate interacting proteins in liver tissue.Results The protein expression differences were detected by IP in two HepG2 groups.The experimental group was infected by lentiviral vector with ATF3 over-expression and the control group was infected by mock-vehicle.Several protein bands with expression diversity were analyzed by protein spectrum,which revealed several candidate proteins that may be related with ATF3.Peptide sequences were analyzed by Mascot software and NCBI database.Combined with the existing literature and our study results,Gelsolin (GSN) was identified as a protein closely interacting with ATF3 and confirmed by co-IP,IHC and WB.Conclusions GSN is identified and verified as an interacting protein with ATF3.ATF3 may function as a suppressor of liver cancer via protein-protein interactions with Gelsolin.