Fig 9. Acetate-augmented HCT116 tumor growth requires Acss2/HIF-2α.

(A) Primary tumor weight as well as (B) primary tumor, (C) lung, and (D) liver metastatic burden in nude mice carrying flank tumors derived from luciferase-expressing stably transformed control knockdown HCT116 cells treated by oral gavage with control or acetate (Acet; triacetin), butyrate (Buty, tributyrin), or propionate (Prop; tripropionin) tri-ester (n = 6/treatment). (E) Primary tumor weight as well as (F) primary tumor, and (G) lung metastatic burden in nude mice treated by oral gavage with control or acetate carrying flank tumors derived from luciferase-expressing stably transformed HIF-2α knockdown HCT116 cells rescued with wild-type (K3) or arginine-lysine substituted mutant (R3) HIF-2α, or stably transformed Acss2 knockdown HCT116 cells rescued with wild-type (WT) or cytosol-restricted mutant (ED) Acss2 (n = 6 or 7/treatment). Luciferase activity was assessed by triplicate measurements of tissue extracts. Comparison within each shRNA knockdown/control rescue pair treated with vehicle or acetate (triacetin) was performed by one-tailed unpaired t test with Welch’s correction for groups of equal sample size or by one-tailed Mann-Whitney test for groups of unequal sample size with reductions indicated (*, P<0.05). Values indicated are means with SD (weights) or SEM (luciferase measurements).