The relative expression degree of SPOCK1 was somewhat higher in tumor tissues compared with their nontumor competitors. SPOCK1 overexpression was detected in 92 of 135 HCCs. Western blotting showed that down-regulation of SPOCK1 protein was detected in 3-9 of 60 randomly selected HCCs. Statistical analysis revealed that HCC tissues expressed a somewhat higher level of SPOCK1 protein than surrounding nontumor tissues. IHC staining was used to study the expression pat-tern of SPOCK1 in paraffin sections from normal liver and matched HCC cells. The expression of SPOCK1 was considerably higher in tumor tissues compared with their adjacent nontumor tissues and normal livers. Interestingly, in some cases, enhanced expression A66 PI3K inhibitor of SPOCK1 was seen in tumor cells at the fringe of the tumor. A clinicopathologic association study in 135 HCCs discovered that overexpression of SPOCK1 was associated significantly with advanced clinical stage and metastasis. HCC people who developed metastasis after hepatectomy showed a significantly higher expression degree of SPOCK1 than those without metastasis, which means that SPOCK1 may play a role in metastasis. More intriguingly, overexpression of SPOCK1 was correlated significantly with shorter over all survival and shorter illness free survival of patients. Multivariate Cox regression analysis further unveiled that SPOCK1 was an independent prognostic marker for the OS time of HCC patients. To examine its function in tumorigenicity, SPOCK1 was cloned into an vector and stably transfected into the HCC cell lines QGY 7703 and PLC 8024. The expression of SPOCK1 in SPOCK1 transfectants was confirmed by Western blot analysis. The power of SPOCK1 was assessed by foci formation, cell growth, and soft agar assays. Compared with empty vector transfected cells, SPOCK1 transfected cells showed greater colonyforming skills in soft agar, and enhanced growth rates, higher foci formation frequencies. To help investigate the in vivo tumorigenic power of SPOCK1, empty vector and SPOCK1 transfected cells were injected subcutaneously into the left and right dorsal flank of nude mice, order GS-1101 respectively. Tumors induced by SPOCK1 7703 transfectants showed notably shorter latency and larger mean tumor size than tumors induced by Vec 7703 cells. An identical result was observed when SPOCK1 transfected PLC 8024 cells were found in the xenograft mouse test. In contrast to the control Vec 8024 cells, SPOCK1 transfected cells showed a dramatically greater mean tumor size. We next examined whether SPOCK1 is required for your phenotypes of HCC cells by silencing SPOCK1 expression with short hairpin RNA against SPOCK1.