Anti-SOX7 (aa 268-388) polyclonal antibody

SOX7 mediates various developmental processes. However, its role in neuronal apoptosis remains unclear. In the present study, we investigated the expression pattern and role of SOX7 in potassium deprivation-induced rat cerebellar granule neuron apoptosis. Our results showed that both mRNA and protein levels of SOX7 were upregulated when potassium was deprived. SOX7 overexpression promoted neuronal apoptosis, whereas knockdown of SOX7 protected neurons against apoptosis. Moreover, we found that -catenin activity was suppressed during apoptosis and that -catenin inhibition was crucial for potassium deprivation-induced neuronal apoptosis. This suppression was mediated by an interaction between SOX7 and -catenin but not by protein degradation. Lastly, we showed that -catenin inhibition mediated the pro-apoptotic effect of SOX7. Together, our findings demonstrated that SOX7 interfered with -catenin activity to promote neuronal apoptosis, which acted as a novel signaling mechanism in neuronal cell death.

The decrease of microRNA-452 (miR-452) in gliomas promoted stem-like features and tumorigenesis. However, the role of miR-452, especially in regulating cancer stem cells (CSCs) in hepatocellular carcinoma (HCC) remains ambiguous. We enriched stem-like HCC cells by serial passages of hepatospheres with chemotherapeutic agents. Stem-like characteristics including the capabilities of chemo-resistance, stemness-related gene expression profiling, self-renewal, tumorigenicity and metastasis formation were detected. MiR-452 was markedly increased in the chemo-resistant hepatospheres and human HCC tissues. and the overexpression of miR-452 in HCC patients predicted poor overall survival. MiR-452 significantly promoted stem-like characteristics in vitro and in vivo. Further, Sox7 was identified as the direct target of miR-452, which could physically bind with beta-catenin and TCF4 in the nucleus and then inhibit the activity of Wnt/beta-catenin signaling pathway. Finally, the combined chemothreapy of doxorubicin and all-trans retinoic acid (ATRA) showed dramatically efficiency in suppressing HCC metastasis. These data suggested that miR-452 promoted stem-like traits of HCC, which might be a potential therapeutic target for HCC. The combination of doxorubicin and ATRA might be a promising therapy in HCC management.