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Studies by Wei and colleagues illustrated that a feed forward mechanism exists between the glucose transporter GLUT1 and the osteoblast transcription factor RUNX2 ( Glut1 promoter ( Figure 3 )

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We found that wild-type (WT) ACTL6A and the DNBL, CC, and NBC ACTL6A mutants reversed the inhibition of cell proliferation and the reduced GCLC protein expression induced by knocking down ACTL6A expression, but the ACTL6A HR-deleted mutant did not show this restorative effect (Fig

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c-Met / proliferation concern is real and unresolved: c-Met is the product of the MET proto-oncogene, and aberrant HGF/c-Met signaling drives several cancers