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. Author manuscript; available in PMC: 2017 Mar 3.
Published in final edited form as: Oncogene. 2016 Aug 22;36(9):1245–1255. doi: 10.1038/onc.2016.290

Figure 7.

Figure 7

c-MYC mediates the cross-talk between HPV and LKB1 in the regulation of HK-II. (a-d) A c-MYC expression construct was transfected into TC-1/shR-Ctrl and TC-1/shR-LKB1 cells and selected with G418 for 2 weeks. (a) Immunoblot blot detection of c-MYC and cell metabolic enzymes in TC-1/shR-Ctrl cells with or without ectopic c-MYC. (b) Extracellular glucose; (c) Extracellular lactate; (d) Intracellular ATP. The data in b-d were the average ± S.D. from 3 independent experiments (*P < 0.01). (e) A model for LKB1-mediated suppression of HPV positive cancer progression by targeting cellular metabolism. The HR HPV infection and the loss of LKB1 collaborate to facilitate transformation of epithelial cells and progression to malignancy.