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. 2020 Mar 10;10:31. doi: 10.1186/s13578-020-00396-1

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Interaction between tumor metabolism and the mTOR signaling pathway. The mTOR pathway is closely related to tumor metabolism. Pathway 1: In bladder cancer, down-regulation of PKM2 expression reduces SREBP-1 expression through inactivated AKT/TSC/Rehb/mTORC1 pathway. The down-regulation of SREBP-1c inhibits FA generation by inhibiting FASN transcription, leading to the inhibition of tumor growth.). Pathway 2: Up-regulation of TEF in tumors activates the Ras/Erk/TSC/Rehb/mTORC1 pathway. Activation of this pathway will promote the uptake of nutrients by tumor cells to meet the needs of the rapid growth of tumors. Pathway 3: HCC can increase sphingomyelin and cardiolipin production by activating mTORC2. Large amounts of sphingomyelin and cardiolipin are used to assemble cell membranes, which also meet the needs of rapid tumor proliferation. Pathway 4: The accumulation of BCAA can promote the occurrence and development of tumors by activating mTORC1. Pathway 5: A2aR, which is highly expressed in gastric cancer, binds adenosine to activate the PI3K/AKT/mTORC1 pathway. Pathway 6: In breast cancer, FFAs promotes tumor proliferation and metastasis by activating the PI3K/AKT/mTORC1 pathway. Pathway 7: The PI3K/AKT/mTORC1/SREBP pathway promotes breast cancer proliferation by inducing new lipid synthesis