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. 2021 Apr 2;15(5):1466–1485. doi: 10.1002/1878-0261.12879

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© 2020 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Fig. 2 — FOXM1D promotes glycolysis. (A, B) ECAR (A) and OCR (B) assays in HeLa cells stably overexpressing FOXM1D and vector control (left panel) and transfected with siRNA specific against FOXM1D or scramble siRNA (right panel). (C) and (D) ECAR (C) and OCR (D) assays in SW‐480 cells stably overexpressing FOXM1D or vector control, and in LoVo cells transfected with siRNA specific against FOXM1D or scramble siRNA. The ectopic expression of FOXM1D enhanced glycolytic activity, while its impaired mitochondrial function. In contrast, the insufficiency of FOXM1D played the opposite role.