ArticleGenes & cancer2012
Oncostatin m promotes mammary tumor metastasis to bone and osteolytic bone degradation.
Article in Genes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 76 citations in OpenAlex.
- TSP-1 interaction with RANK and OPG: implications for bone remodeling and osteolytic bone metastasis.Cell death & disease · 2026Article
- Development of the First Small-Molecule Inhibitor Targeting Oncostatin M for Treatment of Breast Cancer.Journal of medicinal chemistry · 2025Article
- A nomogram for predicting subsequent liver metastasis in patients with metastatic breast cancer.Frontiers in oncology · 2025Article
- PTHrP intracrine actions divergently influence breast cancer growth through p27 and LIFR.Breast cancer research : BCR · 2024Article
- New perspectives in cancer immunotherapy: targeting IL-6 cytokine family.Journal for immunotherapy of cancer · 2023Review
- The clinical relevance of OSM in inflammatory diseases: a comprehensive review.Frontiers in immunology · 2023Review
- Oncostatin M is overexpressed in NASH-related hepatocellular carcinoma and promotes cancer cell invasiveness and angiogenesis.The Journal of pathology · 2022Article
- Stimulation of Osteoclast Formation by Oncostatin M and the Role of WNT16 as a Negative Feedback Regulator.International journal of molecular sciences · 2022Review
- IL-6 Cytokine Family: A Putative Target for Breast Cancer Prevention and Treatment.International journal of molecular sciences · 2022Review
- gp130 Cytokines Activate Novel Signaling Pathways and Alter Bone Dissemination in ER+ Breast Cancer Cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- The IL6-like Cytokine Family: Role and Biomarker Potential in Breast Cancer.Journal of personalized medicine · 2021Review
- Bioactive recombinant human oncostatin M for NMR-based screening in drug discovery.Scientific reports · 2021Article
- Novel mechanism for OSM-promoted extracellular matrix remodeling in breast cancer: LOXL2 upregulation and subsequent ECM alignment.Breast cancer research : BCR · 2021Article
- Interleukins as Mediators of the Tumor Cell-Bone Cell Crosstalk during the Initiation of Breast Cancer Bone Metastasis.International journal of molecular sciences · 2021Review
- Mechanisms forFrontiers in allergy · 2021Article
- Emerging Perspectives on Leukemia Inhibitory Factor and its Receptor in Cancer.Frontiers in oncology · 2021Review
- The Role of Adipokines and Bone Marrow Adipocytes in Breast Cancer Bone Metastasis.International journal of molecular sciences · 2020Review
- GP130 Cytokines in Breast Cancer and Bone.Cancers · 2020Review
- Molecular mechanisms and clinical management of cancer bone metastasis.Bone research · 2020Review
- What Is the Role of Interleukins in Breast Cancer Bone Metastases? A Systematic Review of Preclinical and Clinical Evidence.Cancers · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Oncostatin M (OSM) is an interleukin-6 (IL-6) family cytokine that has been implicated in a number of biological processes including inflammation, hematopoiesis, immune responses, development, and bone homeostasis. Recent evidence suggests that OSM may promote breast tumor invasion and metastasis. We investigated the role of OSM in the formation of bone metastases in vivo using the 4T1.2 mouse mammary tumor model in which OSM expression was knocked down using shRNA (4T1.2-OSM). 4T1.2-OSM cells were injected orthotopically into Balb/c mice, resulting in a greater than 97% decrease in spontaneous metastasis to bone compared to control cells. Intratibial injection of these same 4T1.2-OSM cells also dramatically reduced the osteolytic destruction of trabecular bone volume compared to control cells. Furthermore, in a tumor resection model, mice bearing 4T1.2-OSM tumors showed an increase in survival by a median of 10 days. To investigate the specific cellular mechanisms important for OSM-induced osteolytic metastasis to bone, an in vitro model was developed using the RAW 264.7 preosteoclast cell line co-cultured with 4T1.2 mouse mammary tumor cells. Treatment of co-cultures with OSM resulted in a 3-fold induction of osteoclastogenesis using the TRAP assay. We identified several tumor cell-induced factors including vascular endothelial growth factor, IL-6, and a previously uncharacterized OSM-regulated bone metastasis factor, amphiregulin (AREG), which increased osteoclast differentiation by 4.5-fold. In addition, pretreatment of co-cultures with an anti-AREG neutralizing antibody completely reversed OSM-induced osteoclastogenesis. Our results suggest that one mechanism for OSM-induced osteoclast differentiation is via an AREG autocrine loop, resulting in decreased osteoprotegerin secretion by the 4T1.2 cells. These data provide evidence that OSM might be an important therapeutic target for the prevention of breast cancer metastasis to bone.
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.