Extended Data Fig. 10: AMPKα1 expression levels in tissue microarrays.
From: De novo pyrimidine biosynthetic complexes support cancer cell proliferation and ferroptosis defence
a, b, Tissue microarray staining for AMPKα1 (a) and quantified data of IHC (b). I, liver cancer; II, lung cancer; III, cervical cancer; IV, esophageal cancer; V, colon cancer; VI, gastric cancer; VII, pancreatic cancer. Scale bar, 40 μm. Data are verified in two replicates with similar results(a). Error bars represent mean ± SD, n = 7 biologically independent samples (b). c, A model for the pyrimidinosome under different physiological conditions. Under normal conditions, GOT1, CAD, UMPS, VDAC3 and DHODH form the pyrimidinosome. AMPK interacts with the pyrimidinosome and restricts the association between the components of the complex and de novo synthesis of pyrimidine. When AMPK expression is low, the compactness of the pyrimidine biosynthetic complex is enhanced and de novo synthesis of pyrimidine is promoted. Upon energy stress, AMPK is activated and dissociates from the complex, and thus promoting the association between the components of the complex. Under such conditions, the pyrimidinosome enhances the biosynthesis of OA but not UMP, due to the suppression of UMPS by AMPK, which renders cells more resistant to ferroptosis.
