Evidence map›Paper›PMID 38992688›Full record

ArticleJournal of nanobiotechnology2024

Targeting CSF1R in myeloid-derived suppressor cells: insights into its immunomodulatory functions in colorectal cancer and therapeutic implications.

Xin Tong, Shifeng Qiao, Zhe Dong, Xiaohui Zhao, Xiaxia Du, Wei Niu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

6 authors.

Xin TongDepartment of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, P. R. China.
Shifeng QiaoDepartment of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, P. R. China.
Zhe DongDepartment of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, P. R. China.
Xiaohui ZhaoDepartment of Medical Oncology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, P. R. China.
Xiaxia DuDepartment of Rehabilitation, The Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, P. R. China.
Wei NiuDepartment of Gastroenterology, The First Affiliated Hospital of Jinzhou Medical University, No. 2, Section 5, Renmin Street, Guta District, Jinzhou, Liaoning Province, 121000, P. R. China. niuw@jzmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aimed to investigate the critical role of MDSCs in CRC immune suppression, focusing on the CSF1R and JAK/STAT3 signaling axis. Additionally, it assessed the therapeutic efficacy of LNCs@CSF1R siRNA and anti-PD-1 in combination.

methodsSingle-cell transcriptome sequencing data from CRC and adjacent normal tissues identified MDSC-related differentially expressed genes. RNA-seq analysis comprehensively profiled MDSC gene expression in murine CRC tumors. LNCs@CSF1R siRNA nanocarriers effectively targeted and inhibited CSF1R. Flow cytometry quantified changes in MDSC surface markers post-CSF1R inhibition. RNA-seq and pathway enrichment analyses revealed the impact of CSF1R on MDSC metabolism and signaling. The effect of CSF1R inhibition on the JAK/STAT3 signaling axis was validated using Colivelin and metabolic assessments. Glucose and fatty acid uptake were measured via fluorescence-based flow cytometry. The efficacy of LNCs@CSF1R siRNA and anti-PD-1, alone and in combination, was evaluated in a murine CRC model with extensive tumor section analyses.

resultsCSF1R played a significant role in MDSC-mediated immune suppression. LNCs@CSF1R siRNA nanocarriers effectively targeted MDSCs and inhibited CSF1R. CSF1R regulated MDSC fatty acid metabolism and immune suppression through the JAK/STAT3 signaling axis. Inhibition of CSF1R reduced STAT3 activation and target gene expression, which was rescued by Colivelin. Combined treatment with LNCs@CSF1R siRNA and anti-PD-1 significantly slowed tumor growth and reduced MDSC abundance within CRC tumors.

conclusionCSF1R via the JAK/STAT3 axis critically regulates MDSCs, particularly in fatty acid metabolism and immune suppression. Combined therapy with LNCs@CSF1R siRNA and anti-PD-1 enhances therapeutic efficacy in a murine CRC model, providing a strong foundation for future clinical applications.

Indexed as

Colorectal NeoplasmsMyeloid-Derived Suppressor CellsReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRNA, Small InterferingSTAT3 Transcription FactorAnimalsCell Line, TumorFemaleHumansImmunomodulationJanus KinasesMiceMice, Inbred BALB CProgrammed Cell Death 1 ReceptorReceptor, Macrophage Colony-Stimulating FactorSignal TransductionCSF1R protein, humanCsf1r protein, mouseJanus KinasesProgrammed Cell Death 1 ReceptorReceptor, Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRNA, Small InterferingSTAT3 Transcription FactorAnti-PD-1Colorectal cancerCSF1RFatty acid metabolismImmune suppressionJAK/STAT3LNCs@CSF1R siRNAMyeloid-derived suppressor cells

Identifiers

PMID38992688
PMCPMC11238447

What Socratic holds

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LicenceCC BY
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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 Socratic graph.