Selected article for: "acid metabolism and activate mtorc1"

Author: Li, Dongbo; Ji, Hongfei; Niu, Xingjian; Yin, Lei; Wang, Yiran; Gu, Yucui; Wang, Jinlu; Zhou, Xiaoping; Zhang, Han; Zhang, Qingyuan
Title: Tumor-associated macrophages secrete CC-chemokine ligand 2 and induce tamoxifen resistance by activating PI3K/Akt/mTOR in breast cancer
  • Document date: 2019_12_19
  • ID: yj9mb88g_30
    Snippet: CCL2 secretion has been thought to be dependent on the transcription factor NF-κB, which is activated by TNFα in TME. 44 We tested whether breast cancer cells and macrophages pro- expression independent of NF-κB signaling by dephosphorylating the transcription factor FOXK1. 45 We tested the activation of the mTORC1-FOXK1 pathway in MΦ, MS, and MR and found that activation of the mTORC1-FOXK1 pathway was consistent with the secretion trend of .....
    Document: CCL2 secretion has been thought to be dependent on the transcription factor NF-κB, which is activated by TNFα in TME. 44 We tested whether breast cancer cells and macrophages pro- expression independent of NF-κB signaling by dephosphorylating the transcription factor FOXK1. 45 We tested the activation of the mTORC1-FOXK1 pathway in MΦ, MS, and MR and found that activation of the mTORC1-FOXK1 pathway was consistent with the secretion trend of CCL2 ( Figure 3C ). These results suggest that TNFα and amino acid metabolism in CM activate the NF-κB and mTORC1-FOXK1 pathways of TAM promoting the secretion of CCL2.

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