The MMP23B Search Engine Dash Gadget

Figure 3 In vivo evaluation of therapeutic efficacy of the recombinant Salmonella. A. Tumor growth curves of groups as indicated. B. Tumor doubling time (time for a tumor to double in volume) of different groups. Data are presented as mean �� SD, *p Apoptosis inhibitor Our results showed that VNP-PQE-SPRY2 could significantly inhibit the activation of ERK1/2 MMP23B when compared with the vector group VNP-PQE (Figure 4B). However, VNP-PQE-SPRY1 didn��t show significant inhibition on ERK1/2 phosphorylation, suggesting that SPRY2 is a more efficient agent for melanoma gene therapy. Since the RTK signalling plays a pivotal role in the process of proliferation [20], we next explored the effects of ERK1/2 phosphorylation inhibition on proliferation by using Ki-67 as a marker [21]. Immunohistochemical studies indicated that the Ki-67 index (ratio of the number of positive staining cells to the number of all cells) was significantly deceased when the mice were treated with VNP-PQE-SPRY1 (Figure 4C, ?,4D),4D), which is consistent with the results of decreased ERK1/2 phosphorylation. Therefore, our findings indicated that VNP-PQE-SPRY1 likely suppressed melanoma growth through proliferation inhibition mediated by ERK pathway. Figure 4 S. typhimurium strain VNP20009 carrying SPRY2 expressing plasmid induced down-regulation of ERK phosphorylation and inhibition of proliferation in tumor tissues of mice bearing melanoma. A. Western blotting analysis of the expression of phospho-ERK and ... Discussion Salmonella, a kind of facultative anaerobic bacteria, is increasingly Angiogenesis inhibitor investigated in the tumor targeting therapies because of its characteristic of preferential accumulation in the hypoxic and necrotic areas of tumors [22]. Recent studies have showed the efficacy of Salmonella in delivering many kinds of therapeutic agents to the tumor site [23-26]. However, some therapeutic agents could also be detected in the normal tissues, such as liver and spleen, and thus leaded to unintended damages to these tissues. To further reduce the side effects, we used a hypoxia-induced promoter nirB to drive the expression of genes of interest.