Evidence map›Paper›PMID 39783838›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Metabolic-Immune Suppression Mediated by the SIRT1-CX3CL1 Axis Induces Functional Enhancement of Regulatory T Cells in Colorectal Carcinoma.

Ruiyang Zi, Xiang Zhao, Limei Liu, Yijie Wang, Rui Zhang, Zhiheng Bian, Haoran Jiang, Taorui Liu, Yixin Sun, Han Peng and 9 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. The Yin-Yang balance of SIRT1 and SIRT2 in cancer metabolic remodeling.International journal of biological sciences · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
    Review
  16. Review
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Ruiyang ZiDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.ORCID https://orcid.org/0009-0003-0139-2376
Xiang ZhaoDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.ORCID https://orcid.org/0009-0009-3260-7986
Limei LiuChongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Cancer Hospital, Chongqing University, Chongqing, 400038, China.ORCID https://orcid.org/0009-0004-7014-0831
Yijie WangDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Rui ZhangDepartment of Stem Cell and Regenerative Medicine, Southwest Hospital, Third Military Medical University (Army Medical University), ChongQing, 400038, China.
Zhiheng BianDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Haoran JiangDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Taorui LiuDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Yixin SunDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Han PengDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Xuesong WangDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Fanghao LuDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Chao ZhangDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Fan ZhangDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Qing QinDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Houjie LiangDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Jianjun LiDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.ORCID https://orcid.org/0000-0003-4402-5472
Zhihao WeiDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.ORCID https://orcid.org/0009-0008-4174-9241
Yan DongDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.ORCID https://orcid.org/0000-0002-4018-3839

Funding

National Natural Science Foundation of China 81672856National Natural Science Foundation of China 82203669The General Program of Chongqing Natural Science Foundation CSTB2023NSCQ-MSX0596The General Program of Chongqing Natural Science Foundation CSTB2024NSCQ-MSX0524The General Program of Chongqing Natural Science Foundation cstc2021jcyjmsxmX0687
6 · The paper itself

Abstract

Metabolic reprogramming of tumor cells dynamically reshapes the distribution of nutrients and signals in the tumor microenvironment (TME), affecting intercellular interactions and resulting in metabolic immune suppression. Increased glucose uptake and metabolism are characteristic of many tumors. Meanwhile, the progression of colorectal carcinoma (CRC) relies on lipid metabolism. Therefore, investigating the role of glucolipid metabolic reprogramming on tumor immunity contributes to identifying new targets for immune suppression intervention in CRC. Our previous work demonstrated that SIRT1 is the hub gene involved in glucolipid metabolic conversion in CRC. Here, it is found that upregulated SIRT1 in CRC cells increases Treg functionality by promoting the secretion of CX3CL1. The CX3CL1-CX3CR1 signaling activated transcription factors SATB1 and BTG2, promoting the differentiation of TCF7

Indexed as

Chemokine CX3CL1Colorectal NeoplasmsSirtuin 1T-Lymphocytes, RegulatoryAnimalsCell Line, TumorCX3C Chemokine Receptor 1HumansMiceSignal TransductionTumor MicroenvironmentChemokine CX3CL1CX3C Chemokine Receptor 1CX3CL1 protein, humanSIRT1 protein, humanSirtuin 1Colorectal carcinomaCX3CL1ImmunosuppressionRegulatory T cellSIRT1

Identifiers

PMID39783838
PMCPMC12061293

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.