Fig. 6
- ID
- ZDB-FIG-221106-20
- Publication
- Mohanty et al., 2022 - CRISPR-based kinome-screening revealed MINK1 as a druggable player to rewire 5FU-resistance in OSCC through AKT/MDM2/p53 axis
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Lestaurtinib and 5FU synergistically reduced tumor burden in vivo in drug resistant OSCC.
A Patient-derived cells (PDC2) were earlier established from tumor of chemotherapy (TPF) non-responder patient. PDC2 were implanted in the right upper flank of athymic male nude mice, after which they were treated (i.p) with 5FU and/or Lestaurtinib at indicated concentrations. At the end of the experiment mice were euthanized, and tumors were isolated and photographed (n = 5). B Bar diagram indicates the tumor weight measured at the end of the experiment (mean ± SEM, n = 5). Two-way ANOVA, ****P < 0.0001. C Tumor growth was measured at the indicated time points using digital slide caliper and plotted as a graph (mean ± SEM, n = 5). Two-way ANOVA, ****P < 0.0001. D After completion of treatment, tumors were isolated, and paraffin-embedded sections were prepared as described in Methods to perform IHC with indicated antibodies. Scale bars: 50 μm. E Schematic presentation of the mechanism by which MINK1 regulates p53 expression through AKT/MDM2 axis. |