Fig 1: ABT263 abrogates anti-PD1/exomiR-4315-induced resistance to chemotherapy in an in vivo model of lung cancer.A Cisplatin-induced cell death measure and PARP and Caspase-3 cleavage studies were applied to show that the phenotype of cisplatin resistance induced by exosomes derived from T cells exposed to aPD1 (Exo/aPD1) was abrogated by the use of ABT263.A Cell. B Schematic representation of our in vivo experimentations. C Graph represents the impact of treatment on tumor volume, Bim expression at mRNA (RT-qPCR experiments) and protein (ELIZA, Bim ELIZA Kit MyBioSOURCE#MBS9500064, USA) levels and on the level of serum cytochrome c (Cytochrom C ELIZA kit, Biovision#E4286-100, France). Each treatment included four mice. D Correlation between the impact of treatment on tumor volume and the level of serum cytochrome c in mice.
Fig 2: Exosomal miR-4315 targets Bim.A RT-qPCR and ELIZA were used to analyze the impact of mimic miR-4315, exosomes derived from T cells exposed to the IgG control (Exo) and exosomes derived from T cells exposed to aPD1 (Exo/aPD1) ± antimiR. B The luciferase reporter assay was used to verify that Bim was the target gene of miR-4315. C The graph illustrates the miR-4315 and 3'UTR/Bim enrichments on GW182 and IgG (negative control). Experiments were performed using the RiboCluster Profiler kit (CliniScience, France) according to the manufacturer’s instructions. Experiments were performed 48 h after exosomal exposure.
Fig 3: Exosomes derived from T cells exposed to aPD1 (Exo/aPD1) promote a phenotype of cisplatin-induced apoptosis in A549 cells via miR-4315.Cisplatin-induced cell death measure, PARP and Caspase-3 cleavages were applied to show that exosomes derived from T cells exposed to aPD1 (Exo/aPD1) promote a phenotype of cisplatin-induced apoptosis. RT-qPCR and in-cell ELIZA were applied to show that this phenomenon is associated with the miR-4315-mediated down-regulation of Bim.
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