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. 2020 Mar 2;52(3):409–422. doi: 10.1038/s12276-020-0390-4

Fig. 6. PROM2 augments gemcitabine chemoresistance by binding to Akt.

Fig. 6

a Immunoprecipitation assays showing PROM2 interacts with Akt. b PROM2 binds to Akt endogenously. c Protein expressions of p-BAD and p-Caspase-9 are inhibited when silencing Akt. d IC50 value of gemcitabine in the indicated cells after Akt knockdown (*P < 0.05). e Luminescence signaling of tumors formed by AsPC-1/PROM2 cells after treatment with control or Akt shRNA (*P < 0.05). f Tumor weight of tumors formed by AsPC-1/PROM2 cells after treatment with control or Akt shRNA (*P < 0.05). g Representative images of the immunostaining in tumors tissues (*P < 0.05). h Far-western blotting indicated that Flag-PROM2 interacted with recombinant GST-AKT directly. i Schematic illustration of full length PROM2 and truncations (left) and co-IP assays revealed AKT bound with FL, F1, and F4 fragments, but not with F2 and F3 fragments (right). j Immunoprecipitation assays illustrating the inhibitory effect of PROM2-F4 on the PROM2-AKT interaction. k Quantification of Annexin-V apoptotic cells in indicated cells treated with Gemcitabine (10 μM) (mean ± SD, n = 3; *P < 0.05).