ArticleCarcinogenesis2017
Six1 promotes colorectal cancer growth and metastasis by stimulating angiogenesis and recruiting tumor-associated macrophages.
Article in Carcinogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 86 citations in OpenAlex.
- SIX1 drives acute myeloid leukemia progression by reprogramming glycolytic metabolism and impairing CD8⁺ T-cell effector function.Immunologic research · 2026Article
- A microscopically assisted limited colectomy mouse model of early colon cancer.Animal models and experimental medicine · 2026Article
- CD11dGenes and immunity · 2026Article
- Article
- Senescence-circadian interplay stratifies patient prognosis and reveals immune remodeling heterogeneity in colorectal cancer.Frontiers in immunology · 2026Article
- Effects of Thymidine Phosphorylase and Sine Oculis Homeobox Homologue 1 on the Prognosis and Immune Microenvironment of Gastric Cancer.Current medical science · 2025Article
- Impact of Subcutaneous Versus Orthotopic Implantations on Patient-Derived Xenograft Transcriptomic Profiles.Cancer research communications · 2025Article
- Brd7 loss reawakens dormant metastasis initiating cells in lung by forging an immunosuppressive niche.Nature communications · 2025Article
- Sine oculis homeobox homolog family function in gastrointestinal cancer: Progression and comprehensive analysis.World journal of clinical oncology · 2025Review
- The Role of Macrophages in Various Types of Tumors and the Possibility of Their Use as Targets for Antitumor Therapy.Cancers · 2025Review
- Targeting tumor-associated macrophages in colon cancer: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Research progress of tumor-associated macrophages in immune checkpoint inhibitor tolerance in colorectal cancer.World journal of gastrointestinal oncology · 2024Review
- Article
- Targeting sine oculis homeoprotein 1 (SIX1): A review of oncogenic roles and potential natural product therapeutics.Heliyon · 2024Review
- Crosstalk between colorectal CSCs and immune cells in tumorigenesis, and strategies for targeting colorectal CSCs.Experimental hematology & oncology · 2024Review
- Tumor-associated macrophages in colorectal cancer metastasis: molecular insights and translational perspectives.Journal of translational medicine · 2024Review
- Adipose Mesenchymal Stem Cell-derived Exosomes Enhanced Glycolysis through the SIX1/HBO1 Pathway against Oxygen and Glucose Deprivation Injury in Human Umbilical Vein Endothelial Cells.Current stem cell research & therapy · 2024Article
- SIX1 amplification modulates stemness and tumorigenesis in breast cancer.Journal of translational medicine · 2023Article
- Macrophage's role in solid tumors: two edges of a sword.Cancer cell international · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The homeoprotein Six1 is overexpressed in many human cancers and is associated with increased tumor progression and metastasis. Recent studies have shown that Six1 is associated with poorer overall survival in advanced-stage colorectal cancer (CRC). In the current study, we explored the functional changes and molecular events associated with Six1 overexpression in a mouse model of CRC. An orthotopic model and a splenic injection metastasis model were used to investigate the role of Six1 in CRC tumor growth and metastasis using mouse colon adenocarcinoma MC38 cells overexpressing Six1. We found that overexpression of Six1 dramatically promotes CRC tumor growth and metastasis in vivo. Six1 overexpression in MC38 increased protein levels of aldehyde dehydrogenase-1 and expanded CD44+/CD166+ populations, indicating Six1 increased features of cancer stem cells. In addition, Six1 overexpression stimulated angiogenesis by upregulating the expression of vascular endothelial growth factor (VEGF). Six1-overexpressing tumor cells recruited tumor-associated macrophages (TAM) by increasing the expression of macrophage-specific colony stimulating factor, chemokine (C-C motif) ligand 2/5 and VEGF, further facilitating CRC tumor growth and metastasis. Furthermore, we determined that Six1 activated mitogen-activated protein kinase (MAPK) signaling in CRC cells. In summary, our studies strongly suggest that Six1 overexpression promotes CRC growth and metastasis and remodels tumor stroma by stimulating angiogenesis and recruiting TAM. MAPK activation may be a pivotal event in Six1-associated tumor progression, which may provide opportunities for pharmacologic intervention.
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Registered trials
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.