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. 2019 Mar 20;11(3):393. doi: 10.3390/cancers11030393

Figure 3.

Figure 3

FOXK1/2 transcription factors in the control of metabolic processes. FOXK1/2 transcription factors are phosphorylated by mTOR, which translocate them to the nucleus where they interact with the Sin3A complex to suppress genes involved in atrophy and autophagy programs. Moreover, mTOR induces nuclear translocation of FOXK transcription factors through GSK regulation. In this context, FOXK1/2 induces HIF1α gene expression and glucose consumption, contributing to cell proliferation. Additionally, FOXK1/2 regulate aerobic glycolysis while suppressing aerobic oxidation through the upregulation of glycolytic target genes. mTOR, mammalian target of rapamycin; Gsk3, glycogen synthase kinase 3; HIF1α, hypoxia-inducing factor 1 alpha; SIN3A complex, SIN3 Transcription Regulator Family Member A complex; HK2, hexokinase-2; PFKM, phosphofructokinase muscle isoform; ALDOA, aldolase A; PKM, pyruvate kinase M1/2; MCT1, monocarboxylate transporter 1; PDK1/4, pyruvate dehydrogenase kinases 1/4; PDP1, Pyruvate dehydrogenase phosphatase 1; GLUD1, glutamate dehydrogenase 1; P, phosphorylation site.