ArticleJournal of molecular cell biology2020
Cancer-associated adipocyte-derived G-CSF promotes breast cancer malignancy via Stat3 signaling.
Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
The trial behind it
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Who cites it
33 citing papers in PubMed, 67 citations in OpenAlex.
- Micro-Organ Chip Deciphers Tumor-Derived G-CSF as Remote Commander of Lung Pre-Metastatic Niche via VEGFA-KDR Cascade.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Environmental Lead Promotes Breast Cancer Migration and Invasion via the AKR1C3-NF-κB-MMP Axis.Biomedicines · 2026Article
- G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.European journal of medical research · 2026Article
- CAA-derived IL-6 promoted the PD-L1 expression of breast cancer via STAT3/miR-497a-5p signaling.Journal of cancer research and clinical oncology · 2025Article
- Lactobacillus acidophilus potentiates oncolytic virotherapy through modulating gut microbiota homeostasis in hepatocellular carcinoma.Nature communications · 2025Article
- Cancer-associated fibroblasts secrete CSF3 to promote TNBC progression via enhancing PGM2L1-dependent glycolysis reprogramming.Cell death & disease · 2025Article
- Role, mechanisms and effects ofOncology letters · 2025Review
- Adipokines in Breast Cancer: Decoding Genetic and Proteomic Mechanisms Underlying Migration, Invasion, and Proliferation.Breast cancer (Dove Medical Press) · 2025Article
- ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity.Frontiers in oncology · 2025Article
- Irisin's Dual Role in Malignant Tumors and Its Potential as a Biomarker and Therapeutic Target.Drug design, development and therapy · 2025Review
- Clinical Prognosis and Nomograms for Hormone Receptor-Positive and Human Epidermal Growth Factor Receptor 2-Negative Metastatic Breast Cancer Patients Treated with Palbociclib and Endocrine Therapy.Breast cancer (Dove Medical Press) · 2025Article
- Exploring the therapeutic potential andFrontiers in pharmacology · 2025Article
- Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024Review
- Effect of genistein supplementation on microenvironment regulation of breast tumors in obese mice.Breast cancer research : BCR · 2024Article
- Dissecting the emerging role of cancer-associated adipocyte-derived cytokines in remodeling breast cancer progression.Heliyon · 2024Review
- CSF2 upregulates CXCL3 expression in adipocytes to promote metastasis of breast cancer via the FAK signaling pathway.Journal of molecular cell biology · 2023Article
- Article
- Understanding the mechanisms underlying obesity in remodeling the breast tumor immune microenvironment: from the perspective of inflammation.Cancer biology & medicine · 2023Review
- Dynamic tumor microenvironment, molecular heterogeneity, and distinct immunologic portrait of triple-negative breast cancer: an impact on classification and treatment approaches.Breast cancer (Tokyo, Japan) · 2023Review
- Cancer-Associated Adipocytes and Breast Cancer: Intertwining in the Tumor Microenvironment and Challenges for Cancer Therapy.Cancers · 2023Review
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipocyte is the most predominant cell type in the tumor microenvironment of breast cancer and plays a pivotal role in cancer progression, yet the underlying mechanisms and functional mediators remain elusive. We isolated primary preadipocytes from mammary fat pads of human breast cancer patients and generated mature adipocytes and cancer-associated adipocytes (CAAs) in vitro. The CAAs exhibited significantly different gene expression profiles as assessed by transcriptome sequencing. One of the highly expressed genes in CAAs is granulocyte colony-stimulating factor (G-CSF). Treatment with recombinant human G-CSF protein or stable expression of human G-CSF in triple-negative breast cancer (TNBC) cell lines enhanced epithelial-mesenchymal transition, migration, and invasion of cancer cells, by activating Stat3. Accordantly, targeting G-CSF/Stat3 signaling with G-CSF-neutralizing antibody, a chemical inhibitor, or siRNAs for Stat3 could all abrogate CAA- or G-CSF-induced migration and invasion of breast cancer cells. The pro-invasive genes MMP2 and MMP9 were identified as target genes of G-CSF in TNBC cells. Furthermore, in human breast cancer tissues, elevated G-CSF expression in adipocytes is well correlated with activated Stat3 signal in cancer cells. Together, our results suggest a novel strategy to intervene with invasive breast cancers by targeting CAA-derived G-CSF.
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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.