Anti-CD44 monoclonal antibody, clone VFF-7 [FITC]

Circulating tumor cells (CTCs) represent the most common way of tumor metastasis and has been considered as a significant index for tumor diagnosis, staging and prognosis. However, CTC detection and analysis are always limited by the scarcity of CTC in the peripheral blood and the interference of blood cells. Therefore, here we presented with a hydrogen peroxide (H2O2)-response nanoprobes with CD44-targeted ability to reduce the interference of blood cells and improve the detection efficiency and accuracy and the pancreatic cancer cell was used to evaluate the feasibility of our probe. Shortly, hydrophobic H2O2-response naphthalimide-borate fluorophore was introduced onto the hydrophilic hyaluronic acid to form an amphiphilic complex, which could self-assemble into fluorescent nanoprobes in water. Our studies demonstrated that the nanoprobes were not only able to specifically recognize the pancreatic cancer cells with overexpressed CD44 proteins and reduce the influence of white blood cells in the peripheral blood, but also capable of semi-quantifying H(2)O(2 )content in CTCs, Which could be further used as a significant index for tumor clinical evaluation and therapy.

Chronic NF-kappa B activation in inflammation and cancer has long been linked to persistent activation of NF-kappa B-responsive gene promoters. However, NF-kappa B factors also massively bind to gene bodies. Here, we demonstrate that recruitment of the NF-kappa B factor RELA to intragenic regions regulates alternative splicing upon NF-kappa B activation by the viral oncogene Tax of HTLV-1. Integrative analyses of RNA splicing and chromatin occupancy, combined with chromatin tethering assays, demonstrate that DNA-bound RELA interacts with and recruits the splicing regulator DDX17, in an NF-kappa B activation-dependent manner. This leads to alternative splicing of target exons due to the RNA helicase activity of DDX17. Similar results were obtained upon Tax-independent NF-kappa B activation, indicating that Tax likely exacerbates a physiological process where RELA provides splice target specificity. Collectively, our results demonstrate a physical and direct involvement of NF-kappa B in alternative splicing regulation, which significantly revisits our knowledge of HTLV-1 pathogenesis and other NF-kappa B-related diseases.