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Abstract Tumor cells exploit glucose metabolic reprogramming, most notably the Warburg effect of aerobic glycolysis to fuel rapid proliferation, biosynthetic precursor production, and immunosuppressive microenvironment formation
Integration of metabolic and gene regulatory networks modulates the C
In breast cancer cells, a high level of miR-378* induces the metabolic shift from an oxidative to a glycolytic bioenergetics pathway by inhibiting the expression of two PGC-1 partners, ERR (estrogen-related receptor gamma) and GABPA (GA binding protein transcription factor, alpha subunit)
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