Ibited invasion and migration Caspase Pathway of THP by decreasing the phosphorylation of ERK1 / 2, JNK and p38 MAPK. Although further studies are needed, we recommend that Rh1 is a general inhibitor of invasion and migration through the inhibition of MAPK act. As Rh1 showed an inhibitory effect on MMP 1 expression, we examined the effect of the molecular Rh1 determine whether the transcription factor AP Appendix 1 Rh1inhibits of MMP 1 promoter or inhibits the expression of an AP subunit. PMA induces the activation of MMP-promoter by induction of a Bindungsaktivit T for the proximal AP AP 1 binding site and in the distal AP 1 binding site as shown by EMSA. Rh1 inhibited the expression of AP 1 dimers, c Jun and Fos c, but no influence on the activity t of DNA-binding AP 1 dimers on binding sites AP 1 in the MMP 1 promoter. The observation that Rh1 inhibited PMA-induced MMP 1 transcriptional activity T, without the AP 1 DNA binding obtained Ht the M Possibility that modulate Rh1, a further M Possibility, the activity of t of MMP 1 promoter inhibit. ERK MAPK type are known, in the phosphorylation of c June at several locations, including normal serine 63 and 73 are included. Phosphorylation of these residues leads to a stabilization of c June, and the St Rkung the trans-activating and DNA-binding activity of t. Recent studies describe the integration of C June in the early stages of development of hepatocellular Ren cancer or liver regeneration after partial hepatectomy suggested that the JNK pathway plays a role The key in the expression of MMP gene in a hepatocellular Res carcinoma. The transcriptional activity of t and stability t of c Jun are increased by phosphorylation of serine Hte 63 and 73 by JNK, w While phosphorylation on threonine 91 and 93 June resulted in enhanced c-DNA binding. In addition, the phosphorylation proposed by the same sites to hen the stability t of the protein obtained by the inhibition of ubiquitin, Resulting in a slight increase in their equilibrium state. In this way, the activation of ERK1 / 2 has been shown, C June expression and stability to induce t, indicating cross talk between ERK1 / 2 and JNK pathways regulating the activity of t of c in June Therefore, we studied the effect of Rh1 on the stability t of c in June under conditions of cycloheximide treatment in the presence or absence of 100 M Rh1. Rh1 reduced the stability t of c in June compared to controls of vehicles. Therefore, antimetastatic activity t Rh1 in HepG2 cells through inhibition of MMP-1 by inhibiting the expression of a phrase AP dimer, and the attenuator Monitoring the stability of t c from June through inhibition of phosphorylation of ERK and JNK. However, we have the M Not rule out possibility S that Rh1 in the inhibition of binding to an AP-1 MMP promoter, such as Rh1 inhibited the mobility Ts-shift of a common binding oligomer AP k can be involved. To best term Whether other AP-1 binding sites in the MMP-1 promoter in the expression of MMP 1 are involved, further studies are conducted to determine the molecular function of Rh1. In summary, treatment with Rh1, an anti-metastatic to create by the inhibition of MMP-1 transcriptional activity of t and the expression and stability t of the dimeric AP 1, c Fos and c-jun by inhibiting JNK and ERK1 / 2 activation in HepG2 cells. The results of this study suggest that Rh1 has potential.