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These data suggest that THAP11 inhibited CD44 v6 expression depending on the interaction with PCBP1. We further investigated whether THAP11 affected the tumor cell invasion. PCBP1 or THAP11 expression vector was transfected into HepG2 cells and cell invasion was measured. The cell invasion of PCBP1 transfected cells was about 67% of the control cells, while THAP11 overexpression led to about 52% decrease of the cell invasion compared to the control (Fig. 5A and B). Co-expression of THAP11 and PCBP1 led to almost 90% reduction of cell invasion, suggesting a synergistic effect between THAP11 and PCBP1. The similar results were obtained in SMMC-7721 cells (Fig. S4) and HCT116 cells (Fig. S5). To confirm the effect of THAP11 selleck kinase inhibitor on cell invasion, endogenous THAP11 was knockdown by RNAi and then cell invasion was measured. As shown in Fig. 5C and D, knockdown of THAP11 in HepG2 cells led to about 2.1-fold increased of cell invasion. The similar results were obtained in SMMC-7721 cells (data not shown). These results suggested Megestrol Acetate that THAP11 negatively regulated tumor cell invasion, which is similar to PCBP1. Since both PCBP1 and THAP11 are negative regulators in tumor cell invasion and down-regulated in HCC tissues, we further examined whether a correlation of the expression pattern of THAP11 and PCBP1 exists in primary HCC. Real-time PCR analysis was performed to detect the mRNA levels of THAP11 and PCBP1 (Fig. S6) in HCC tissues and the adjacent non-cancerous liver tissues of 33 HCC patients. The result suggested that in HCC tissues, THAP11 mRNA expression showed significant correlation with the expression of PCBP1 mRNA (n?=?33, r?=?0.847, p?Selleck UMI-77 on v6 expression in detail. Overexpression of THAP11 in HepG2 cells can inhibit the v6 expression induced by Ras activation and HGF, and knockdown of endogenous THAP11 led to increased level of v6 mRNA. Furthermore, overexpression of THAP11 markedly inhibited the tumor cell invasion while knockdown of THAP11 increased the cell invasion. These results indicate that THAP11 is a novel negative regulator of CD44 variant splicing and tumor cell invasion. Since no evidence suggests that THAP11 has the activity of binding RNA, it is easy to hypothesize that THAP11 regulates v6 splicing by association with other trans-acting factors.