ArticleCancer research2009
Lack of Muc1-regulated beta-catenin stability results in aberrant expansion of CD11b+Gr1+ myeloid-derived suppressor cells from the bone marrow.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Interplay between Signaling Pathways and Tumor Microenvironment Components: A Paradoxical Role in Colorectal Cancer.International journal of molecular sciences · 2023Review
- Repression of MUC1 Promotes Expansion and Suppressive Function of Myeloid-Derived Suppressor Cells in Pancreatic and Breast Cancer Murine Models.International journal of molecular sciences · 2021Article
- MicroRNA 449c Mediates the Generation of Monocytic Myeloid-Derived Suppressor Cells by Targeting STAT6.Molecules and cells · 2020Article
- Membrane-associated mucins of the ocular surface: New genes, new protein functions and new biological roles in human and mouse.Progress in retinal and eye research · 2020Review
- Granulocytic Myeloid-Derived Suppressor Cells as Negative Regulators of Anticancer Immunity.Frontiers in immunology · 2020Review
- Wnt Signaling Cascade in Dendritic Cells and Regulation of Anti-tumor Immunity.Frontiers in immunology · 2020Review
- New therapeutic targets for cancer: the interplay between immune and metabolic checkpoints and gut microbiota.Clinical and translational medicine · 2019Review
- CXCR2 expression on granulocyte and macrophage progenitors under tumor conditions contributes to mo-MDSC generation via SAP18/ERK/STAT3.Cell death & disease · 2019Article
- Mucin-1 is required for Coxsackie Virus B3-induced inflammation in pancreatitis.Scientific reports · 2019Article
- WNT Signaling in Cancer Immunosurveillance.Trends in cell biology · 2019Review
- WNT/β-Catenin Signaling Pathway Regulating T Cell-Inflammation in the Tumor Microenvironment.Frontiers in immunology · 2019Review
- MUC1 Mucin: A Putative Regulatory (Checkpoint) Molecule of T Cells.Frontiers in immunology · 2018Review
- Regulation of gene expression in the bovine blastocyst by colony stimulating factor 2.BMC research notes · 2016Article
- Genetically engineered mucin mouse models for inflammation and cancer.Cancer metastasis reviews · 2015Review
- MUC1 (CD227): a multi-tasked molecule.Cellular and molecular life sciences : CMLS · 2015Review
- Pancreatic Cancer Cells Isolated from Muc1-Null Tumors Favor the Generation of a Mature Less Suppressive MDSC Population.Frontiers in immunology · 2014Article
- Downregulation of hematopoietic MUC1 during experimental colitis increases tumor-promoting myeloid-derived suppressor cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Transmembrane mucin MUC1 overexpression and its association with CD10⁺ myeloid cells, transforming growth factor-β1 expression, and tumor budding grade in colorectal cancer.Cancer science · 2013Article
- A novel role of hematopoietic CCL5 in promoting triple-negative mammary tumor progression by regulating generation of myeloid-derived suppressor cells.Cell research · 2013Article
- Cellular and molecular biology of airway mucins.International review of cell and molecular biology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of myeloid cells that inhibit T-cell activity and contribute to the immune suppression characteristic of most tumors. We discovered that bone marrow (BM) progenitor cells from the Muc1 knockout (KO) mice differentiated into CD11b(+)Gr1(+) MDSCs in vitro under granulocyte macrophage colony-stimulating factor and interleukin-4 signaling. MUC1 is a tumor-associated mucin and its cytoplasmic tail (MUC1-CT) can regulate beta-catenin to promote oncogenesis. Given the importance of beta-catenin in hematopoiesis, we hypothesized that the MUC1 regulation of beta-catenin is important for MDSC development. Our current study shows that the aberrant development of BM progenitors into CD11b(+)Gr1(+) MDSCs is dependent on the down-regulation of beta-catenin levels that occurs in the absence of Muc1. In light of this, KO mice showed enhanced EL4 tumor growth and were able to better tolerate allogeneic BM185 tumor growth, with an accumulation of CD11b(+)Gr1(+) cells in the blood and tumor-draining lymph nodes. WT mice were able to similarly tolerate allogeneic tumor growth when they were injected with CD11b(+)Gr1(+) cells from tumor-bearing KO mice, suggesting that tolerance of allogeneic tumors is dependent on MDSC-mediated immune suppression. This further delineates the ability of Muc1 to control MDSC development, which could directly affect tumorigenesis. Knowledge of the biology by which Muc1 regulates the development of myeloid progenitors into MDSCs would also be very useful in enhancing the efficacy of cancer vaccines in the face of tumor immune suppression.
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.