Extended Data Fig. 2: Dysplastic cancer cells presented increased glycolysis in an in vivo model of cutaneous SCC and in human HNSCC in the context of SIRT6.
From: A unique subset of glycolytic tumour-propagating cells drives squamous cell carcinoma

Extended Data Fig. 2 (related to Fig. 1)a, H&E stained images of early SCC found only among Sirt6 cKO tumours. Scale bars indicate 200µm b, PCNA (top) and GLUT1 (bottom) immunostaining in normal untreated skin, P27 anagen animal back skin, and dysplastic skin treated with DMBA/TPA. Dashed line indicates either hair follicle or epidermis. For normal skin, both images came from the same untreated mouse, but not immediate adjacent skin sections. Scale bars indicate 100µm. Immunostaining was performed ten times for GLUT1 and six times for PCNA with similar results. c, Glut1 and Ldha expression in normal skin and skin tumors from Sirt6-deficient animals at 21 weeks after DMBA treatment. Data indicate mean ± S.E.M. Each dot represents one biologically independent tumour sample. (n = 1, 2, 6, 5, respectively, from left to right in each graph) Student’s t-tests were performed (two-sided). d, GLUT1, phospho-PDH (Ser293), and MPC1 immunostaining in Sirt6-deleted large papilloma samples. Scale bars indicate 100µm. e, SIRT6, GLUT1, PDK1, and LDHB expression levels in human HNSCC compared by tumour grade from Ginos et al. listed in the Oncomine. Immunostaining against GLUT1, p-PDH, and MPC1 was performed ten, three, and two times, respectively, with similar results. f, Representative SIRT6 and GLUT1 immunostaining from human differentiated HNSCC and undifferentiated HNSCC. Immunostaining was performed two times with similar results. Scale bars indicate 100µm. * p<0.05 ** p<0.01.