ArticleExperimental cell research2009
Both cell-surface and secreted CSF-1 expressed by tumor cells metastatic to bone can contribute to osteoclast activation.
Article in Experimental cell research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Two-sample Mendelian randomization analysis of the causal association between circulating inflammatory proteins and osteosarcoma.Discover oncology · 2025Article
- Energy stress and adaptation strategy of tumor cells in different microenvironments: from primary tumors to distant metastases.Acta biochimica et biophysica Sinica · 2025Review
- Pharmacologic Hedgehog inhibition modulates the cytokine profile of osteolytic breast cancer cells.Journal of bone oncology · 2024Article
- Decreased melanoma CSF-1 secretion by Cannabigerol treatment reprograms regulatory myeloid cells and reduces tumor progression.Oncoimmunology · 2023Article
- Bone marrow niches in the regulation of bone metastasis.British journal of cancer · 2021Review
- Molecular insights into the interplay between adiposity, breast cancer and bone metastasis.Clinical & experimental metastasis · 2021Review
- The M-CSF receptor in osteoclasts and beyond.Experimental & molecular medicine · 2020Review
- Cytokine mediators of chronic graft-versus-host disease.The Journal of clinical investigation · 2017Review
- High fat diet increases melanoma cell growth in the bone marrow by inducing osteopontin and interleukin 6.Oncotarget · 2016Article
- Molecular regulation of bone marrow metastasis in prostate and breast cancer.Bone marrow research · 2014Review
- Article
- Prognostic impact of CD57, CD68, M-CSF, CSF-1R, Ki67 and TGF-beta in soft tissue sarcomas.BMC clinical pathology · 2012Article
- A short account of metastatic bone disease.Cancer cell international · 2011Article
- Protective role of osteopontin in endodontic infection.Immunology · 2010Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tumors metastatic to the bone produce factors that cause massive bone resorption mediated by osteoclasts in the bone microenvironment. Colony stimulating factor (CSF-1) is strictly required for the formation and survival of active osteoclasts, and is frequently produced by tumor cells. Here we hypothesize that the CSF-1 made by tumor cells contributes to bone destruction in osteolytic bone metastases. We show that high level CSF-1 protected osteoclasts from suppressive effects of transforming growth factor beta (TGF-beta). r3T cells, a mouse mammary tumor cell line that forms osteolytic bone metastases, express abundant CSF-1 in vitro as both a secreted and a membrane-spanning cell-surface glycoprotein, and we show that both the secreted and the cell-surface form of CSF-1 made by r3T cells can support osteoclast formation in co-culture experiments in the presence of RankL. Mice with r3T bone metastases have elevated levels of both circulating and bone-associated CSF-1, and the majority of CSF-1 found in bone metastases is associated with the tumor cells. These results support the idea that tumor-cell produced CSF-1 contributes to osteoclast development and survival in bone metastasis.
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