ArticleCell death and differentiation2019
Gut microbiota-stimulated cathepsin K secretion mediates TLR4-dependent M2 macrophage polarization and promotes tumor metastasis in colorectal cancer.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 241 papers.
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Who cites it
241 citing papers in PubMed, 379 citations in OpenAlex.
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- Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies.Biomarker research · 2026Review
- Microbial Dynamics across Molecular Subtypes and Prognostic Significance of Lactobacillus in Gastric Cancer.Cancer research and treatment · 2026Article
- The pro-metastatic role of microbiota in tumors: a comprehensive review.Cancer cell international · 2026Review
- Mechanism of enteral nutrition in regulating Tfh/Tfr immune imbalance in colorectal cancer via the TLR4 signaling pathway.Journal of clinical biochemistry and nutrition · 2026Article
- The Gut-Bone Axis: A Systematic Review on the Potential Intervention Pathways for Bone Health.Life (Basel, Switzerland) · 2026Review
- Microbiomics: Novel Biomarkers of Colorectal Cancer Diagnosis and Prognosis.Diagnostics (Basel, Switzerland) · 2026Review
- [Fecal microbiota transplantation inhibits colonic tumor growth in mice by suppressing the TLR4/MyD88/NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Lactobacillus crispatus attenuates Escherichia coli-induced inflammation and migration of cervical cancer cells.AMB Express · 2026Article
- Intestinal obstruction impairs the antitumor function of hepatic natural killer cells against colorectal cancer.Journal of gastroenterology · 2026Article
- Key molecular mechanisms and regulatory networks in colorectal cancer liver metastasis.Biological procedures online · 2026Review
- Unraveling the Link Between Azathioprine and Acute Pancreatitis: Integrating Network Toxicology, Machine Learning, and Mendelian Randomization.CPT: pharmacometrics & systems pharmacology · 2026Article
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Tumor-derived neutrophil extracellular trap-associated DNA impairs treatment efficacy in breast cancer via CCDC25-dependent epithelial-mesenchymal transition.The Journal of clinical investigation · 2026Article
- Integrative multi-omics analysis prioritizes compartment-specific candidate targets of gut microbiota metabolites in diabetic kidney disease.Frontiers in immunology · 2026Article
- Toll-like receptors: versatile players in tumor.Frontiers in immunology · 2026Review
- Relationship between cathepsin K and extracellular matrix dynamics: a comprehensive review.Frontiers in oncology · 2026Review
- Macrophage-Based Nanoplatforms for Tumor-Targeted Drug Delivery and Cancer Immunomodulation: Extracellular Vesicles, Membrane-Coated Nanoparticles, and Live Cells.International journal of nanomedicine · 2026Review
181 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis is a complex process that requires the interaction between tumor cells and their microenvironment. As an important regulator of intestinal microenvironment, gut microbiota plays a significant role in the initiation and progression of colorectal cancer (CRC), but the underlying mechanisms remain elusive. In this study, a metastasis-related secretory protein cathepsin K (CTSK) was identified as a vital mediator between the imbalance of intestinal microbiota and CRC metastasis. We implanted MC38 cells into the cecal mesentry of antibiotic-treated mice with intragastrically administration of E. coli to mimic gut microbiota imbalance. The bigger primary tumors and more liver metastatic foci were detected in the E. coli group accompanied with high LPS secretion and CTSK overexpression compared with that in the control group. CTSK contributes to the aggressive phenotype of CRC cells both in vitro and in vivo. Silencing CTSK or administration of Odanacatib, a CTSK-specific inhibitor, totally abolished the CTSK-enhanced migration and motility of CRC cells. Interestingly, the tumor-secreted CTSK could bind to toll-like receptor 4 (TLR4) to stimulate the M2 polarization of tumor-associated macrophages (TAMs) via an mTOR-dependent pathway. Recombinant CTSK could neither stimulate CRC growth and metastasis, nor induce M2 macrophage polarization in TRL4
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