Anti-SOX7 monoclonal antibody Made to order

Objective: To investigate whether miR-202 regulate the proliferation of prostate cancer (PC) via SOX7 gene. Methods: Real-time quantitative PCR analysis was performed to observe the expression level of miR-202 in three PC cell lines (DU145, PC3, and LNCaP) and issues. Then, miR-202 mimic and the negative control were transfected to DU145, PC3 cell lines to explore the relationship between miR-202 and the proliferation of the PC cells in vitro. Meanwhile, bioinformatical prediction was performed to discover the target gene of the miR-202 (SOX7) which was confirmed by luciferase reporter assay. Moreover, the DU145 and PC3 cell lines were transfected with siRNA-SOX7 or the negative control to confirm the influence of SOX7 on the proliferation of PC. Additionally, the proliferation assay of PC3 cells adopted MTT method. Results: miR-202 expression was up-regulated in PC cell lines and tissues. The MTT assay revealed that the over-expression of miR-202 significantly promoted the proliferation of the PC cells in vitro. The SOX7 was the direct target of the miR-202 and miR-202 down-regulated the expression of SOX7 which was confirmed by the luciferase reporter assay. The knockdown of SOX7 remarkably promoted the proliferation of PC cells in vitro that verified by the MTT assay. Conclusion: The miR-202 could promote the proliferation of PC by targeting the SOX7, indicating a new potential therapeutic target and treatment for the PC.

Cells of the primitive endoderm (PrE) and the pluripotent epiblast (EPI), the two lineages specified within the inner cell mass (ICM) of the mouse blastocyst stage embryo, are segregated into adjacent tissue layers by the end of the preimplantation period. The PrE layer which emerges as a polarized epithelium adjacent to the blastocoel, with a basement membrane separating it from the EPI, has two derivatives, the visceral and parietal endoderm. In this study we have investigated the localization of two transcriptional regulators of the SOX family, SOX17 and SOX7, within the PrE and its derivatives. We noted that SOX17 was first detected in a salt-and-pepper distribution within the ICM, subsequently becoming restricted to the nascent PrE epithelium. This dynamic distribution of SOX17 resembled the localization of GATA6 and GATA4, two other PrE lineage-specific transcription factors. By contrast, SOX7 was only detected in PrE cells positioned in contact with the blastocoel, raising the possibility that these cells are molecularly distinct. Our observations support a model of sequential GATA6 > SOX17 > GATA4 > SOX7 transcription factor activation within the PrE lineage, perhaps correlating with the consecutive periods of cell lineage 'naivete', commitment and sorting. Furthermore our data suggest that co-expression of SOX17 and SOX7 within sorted PrE cells could account for the absence of a detectable phenotype of Sox17 mutant blastocysts. However, analysis of implantation-delayed blastocysts, revealed a role for SOX17 in the maintenance of PrE epithelial integrity, with the absence of SOX17 leading to premature delamination and migration of parietal endoderm. (C) 2010 Published by Elsevier Inc.