| Autor: |
Yiwei Chu, Xi Chen, Jiongbo Liao, Yun Lu, Huanrong Liu, Xiao Wang, Yan Zhang, Hui Yang, Bo Shen, Yujing Bi, Guangwei Liu |
| Rok vydání: |
2023 |
| DOI: |
10.1158/0008-5472.22401441 |
| Popis: |
PDF file - 436K, Fig.S1. MDSC polarizing differentiation condition alters glycolytic activity. Fig.S2.MDSC SIRT1 expansions in spleen and tumor of SIRT1KO and WT-bearing tumor mice. Fig.S3.SIRT1 deficiency MDSCs showed normal cell death and proliferation. Fig.S4.SIRT1 is required for MDSC polarization. Fig.S5.Characterization of surface marker of bone marrow-derived MDSCs. Fig.S6.SIRT1 intrinsicly controls the function and differentiation of tumor MDSCs. Fig.S7.The potentiating killing activity of SIRT1-/- MDSCs is associated with the higher glycolytic activity. Fig.S8.CD115+ monocytic MDSC effects in tumor killing. Fig.S9.SIRT1 deficiency from MDSCs could not alter the activation of NF-κB signaling after LPS treatment. Fig.S10.SIRT1-dependent MDSC glycolytic activity changes are associated with mTOR-HIF1α pathway. Fig.S11.SIRT-HIF axis directs the function and fate of MDSC associated with glycolytic activity. Fig.S12.SIRT-HIF axis potentiates glycolytic activity and tumor killing ability. Fig.S13.SIRT1 masters MDSC function and fate in tumor through mTOR/HIF1α dependent glycolytic pathway. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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