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. 2015 Mar 12;6(13):10880–10892. doi: 10.18632/oncotarget.3534

Figure 5. Knockdown of PIM1 suppressed the glycolytic metabolism in SMMC-7721, possibly through the regulation of p-AKT.

Figure 5

Figure 5

(A) Glucose uptake experiment using 2-NBDG flow cytometry analyses (left panel) and relative glucose uptake (right panel). (B) Expression of p-AKT, total AKT and pyruvate kinase M2 (PKM2) in SMMC-7721 stable PIM1 knockdown clones shPIM1-4 and shPIM1-5. N: normoxia (20% O2) H: hypoxia (1% O2). (C) Expression of GLUT-1 and PKM2 by qPCR in PIM1 stable knockdown clones of SMMC-7721. (D) Immunohistochemical staining of PIM1 and GLUT-1 of HCC tissues in NTC and PIM1 knockdown (KD) clones from subcutaneous inoculation (SMMC-7721) and (E) orthotopic implantation (MHCC-97L) of nude mice. (F) Expression of PIM1, p-AKT, total AKT and PKM2 of SMMC-7721 tumor lysates from NTC and shPIM1-5 after subcutaneous inoculation in nude mice.