Figure 5.

GOT2 acetylation promotes tumor growth, and GOT2 K159 acetylation is increased in pancreatic cancer

• A–C GOT2 3K acetylation promotes xenograft tumor growth. Panc-1 stable cells with GOT2 knockdown and re-expressing the indicated proteins (2 × 10⁶ cells) were injected subcutaneously into the flanks of nude mice. The tumor volume was carefully monitored over the indicated time period (A). At 8 weeks after injection, tumors from six mice were extracted, photographed, and weighted (B, C).
• D GOT2 3K acetylation promotes tumor cell proliferation. Tumor sections from xenografts were prepared for IHC staining, and the PCNA-stained tumor sections were analyzed by quantifying the PCNA-positive area.
• E Clinical cases with increased GOT2 K159 acetylation in human pancreatic tumor tissues. 10 pairs of human pancreatic tumor tissue (shown as T) and adjacent normal tissue (shown as N) were lysed. The acetylation level of GOT2 at K159 was compared against GOT2 protein by Western blot.
• F Clinical cases with decreased SIRT3 protein expression in human pancreatic tumor tissues. 10 pairs of human pancreatic tumor tissue (shown as T) and adjacent normal tissue (shown as N) were lysed. The SIRT3 protein levels were compared against tubulin by Western blot.
• G,H Quantification of GOT2 K159 acetylation and SIRT3 protein expression in clinical cases as described in (E) and (F).

Data information: Shown are average values with standard deviation (SD) of triplicated experiments. *P < 0.05, **P < 0.01, and ***P < 0.001 for the indicated comparison; n.s. = not significant.