ArticleOncogene2013
Macrophage cathepsin K promotes prostate tumor progression in bone.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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.
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.
Who cites it
50 citing papers in PubMed, 90 citations in OpenAlex.
- Cathepsin Family Proteases in Prodrug Design: Recent Advances.ChemMedChem · 2026Review
- Cutting to the core: Proteases in the tumor-bone interface and metastatic progression.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Characterization and validation of a bone metastatic castration-resistant prostate cancer model as a nanomedicine evaluation platform.Theranostics · 2026Article
- Per- and polyfluorinated substances (PFAS) promote osteoclastogenesis and bone loss through PPARα activation.Toxicology reports · 2025Article
- The multifaceted roles of cathepsins in immune and inflammatory responses: implications for cancer therapy, autoimmune diseases, and infectious diseases.Biomarker research · 2024Review
- The potential contribution of aberrant cathepsin K expression to gastric cancer pathogenesis.Discover oncology · 2024Article
- Multiple influence of immune cells in the bone metastatic cancer microenvironment on tumors.Frontiers in immunology · 2024Review
- The Potential of Extracellular Matrix- and Integrin Adhesion Complex-Related Molecules for Prostate Cancer Biomarker Discovery.Biomedicines · 2023Review
- Single-cell multi-omics analysis of human testicular germ cell tumor reveals its molecular features and microenvironment.Nature communications · 2023Article
- Review
- Bone Metastases and Health in Prostate Cancer: From Pathophysiology to Clinical Implications.Cancers · 2023Review
- Cysteine Cathepsins as Therapeutic Targets in Immune Regulation and Immune Disorders.Biomedicines · 2023Review
- Highly potent inhibitors of cathepsin K with a differently positioned cyanohydrazide warhead: structural analysis of binding mode to mature and zymogen-like enzymes.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Cathepsin K in Pathological Conditions and New Therapeutic and Diagnostic Perspectives.International journal of molecular sciences · 2022Review
- Enzyme-Activatable Chemokine Conjugates for In Vivo Targeting of Tumor-Associated Macrophages.Angewandte Chemie (Weinheim an der Bergstrasse, Germany) · 2022Article
- Enzyme-Activatable Chemokine Conjugates for In Vivo Targeting of Tumor-Associated Macrophages.Angewandte Chemie (International ed. in English) · 2022Article
- Lysosomal peptidases-intriguing roles in cancer progression and neurodegeneration.FEBS open bio · 2022Review
- Helicobacter pylori and gastric cancer: a lysosomal protease perspective.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Review
- Differentiation of Cells Isolated from Human Femoral Heads into Functional Osteoclasts.Journal of developmental biology · 2022Article
- Role of lysosomes in physiological activities, diseases, and therapy.Journal of hematology & oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bone marrow macrophages (BMMs) share common progenitors with osteoclasts and are critical components of bone-tumor microenvironment; however, their function in prostate tumor growth in the skeleton has not been explored. BMMs are the major source of inflammatory factors and proteases, including cysteine protease cathepsin K (CTSK). In this study, utilizing mice deficient in CTSK, we demonstrate the critical involvement of this potent collagenase in tumor progression in bone. We present the evidence that tumor growth and progression in the bone are impaired in the absence of CTSK. Most importantly, we show for the first time that BMM-supplied CTSK may be involved in CCL2- and COX-2-driven pathways that contribute to tumor progression in bone. Together, our data unravel novel roles for CTSK in macrophage-regulated processes, and provide evidence for close interplay between inflammatory, osteolytic and tumor cell-driven events in the bone-tumor microenvironment.
Indexed as
Identifiers
What OpenQuestion holds
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.