ArticlePloS one2014
Macrophages mediate a switch between canonical and non-canonical Wnt pathways in canine mammary tumors.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- In vitro comparative models for canine and human breast cancers.Clujul medical (1957) · 2016Review
- Immune Cells in Cancer Therapy and Drug Delivery.Mediators of inflammation · 2016Review
- The Therapeutic Aspects of the Endocannabinoid System (ECS) for Cancer and their Development: From Nature to Laboratory.Current pharmaceutical design · 2016Review
- Human breast cancer cells educate macrophages toward the M2 activation status.Breast cancer research : BCR · 2015Article
- Establishment and characterization of a new cell line of canine inflammatory mammary cancer: IPC-366.PloS one · 2015Article
- Prognostic value of tumor-associated macrophages according to histologic locations and hormone receptor status in breast cancer.PloS one · 2015Article
- Ligand-independent canonical Wnt activity in canine mammary tumor cell lines associated with aberrant LEF1 expression.PloS one · 2014Article
- MDSCs mediate angiogenesis and predispose canine mammary tumor cells for metastasis via IL-28/IL-28RA (IFN-λ) signaling.PloS one · 2014Article
- Article
Corrections and comments
- Retraction · 2019-01-10Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image ·
- Retracted
Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAccording to the current hypothesis, tumor-associated macrophages (TAMs) are "corrupted" by cancer cells and subsequently facilitate, rather than inhibit, tumor metastasis. Because the molecular mechanisms of cancer cell-TAM interactions are complicated and controversial we aimed to better define this phenomenon. METHODS AND
resultsUsing microRNA microarrays, Real-time qPCR and Western blot we showed that co-culture of canine mammary tumor cells with TAMs or treatment with macrophage-conditioned medium inhibited the canonical Wnt pathway and activated the non-canonical Wnt pathway in tumor cells. We also showed that co-culture of TAMs with tumor cells increased expression of canonical Wnt inhibitors in TAMs. Subsequently, we demonstrated macrophage-induced invasive growth patterns and epithelial-mesenchymal transition of tumor cells. Validation of these results in canine mammary carcinoma tissues (n = 50) and xenograft tumors indicated the activation of non-canonical and canonical Wnt pathways in metastatic tumors and non-metastatic malignancies, respectively. Activation of non-canonical Wnt pathway correlated with number of TAMs.
conclusionsWe demonstrated that TAMs mediate a "switch" between canonical and non-canonical Wnt signaling pathways in canine mammary tumors, leading to increased tumor invasion and metastasis. Interestingly, similar changes in neoplastic cells were observed in the presence of macrophage-conditioned medium or live macrophages. These observations indicate that rather than being "corrupted" by cancer cells, TAMs constitutively secrete canonical Wnt inhibitors that decrease tumor proliferation and development, but as a side effect, they induce the non-canonical Wnt pathway, which leads to tumor metastasis. These data challenge the conventional understanding of TAM-cancer cell interactions.
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