Delineating CSF-1-dependent regulation of myeloid cell diversity in tumors

Casbon, Amy-Jo; Lohela, Marja; Werb, Zena

doi:10.1080/2162402x.2015.1008871

Cited by 5 publications

(4 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The presence of PMN-MDSCs in tumors is associated with induction of chronic inflammation and antigen-specific tolerance by T cells (Marigo et al 2010). Using the MMTV-PyMT transgenic breast cancer model, we described that the production of tumor-derived G-CSF during tumor progression induces the systematic differentiation and activation of PMN-MDSCs, characterized by CD11b + Rb1lo Ly6G + (Casbon et al 2015).…”

Section: Neutrophilsmentioning

confidence: 99%

Roles of the immune system in cancer: from tumor initiation to metastatic progression

2018

Self Cite

View full text Add to dashboard Cite

The presence of inflammatory immune cells in human tumors raises a fundamental question in oncology: How do cancer cells avoid the destruction by immune attack? In principle, tumor development can be controlled by cytotoxic innate and adaptive immune cells; however, as the tumor develops from neoplastic tissue to clinically detectable tumors, cancer cells evolve different mechanisms that mimic peripheral immune tolerance in order to avoid tumoricidal attack. Here, we provide an update of recent accomplishments, unifying concepts, and future challenges to study tumor-associated immune cells, with an emphasis on metastatic carcinomas.

show abstract

Section: Neutrophilsmentioning

confidence: 99%

Roles of the immune system in cancer: from tumor initiation to metastatic progression

2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…Inhibition of colony-stimulating factor-1 (CSF-1, also known as M-CSF), the primary regulator of tissue macrophage production, or the blockade of CSF-1 receptor (also known as CD115 or c-fms) led to decreased macrophage infiltration and less mammary tumor growth [ 50 ]. Depletion of CD115 + F4/80 + macrophages during early hyperplastic stage with anti-CSF-1R antibody (M279) reduced primary tumor growth and lung metastasis [ 51 ]. CSF-1 influences also the maturation of tumor-associated macrophages; in CSF-1 deficient animals macrophages remained more immature with lower expression of IL-1 β , TNF- α [ 52 ].…”

Section: Extracellular Signals Driving the Recruitment And Functiomentioning

confidence: 99%

Inflammation and Cancer: Extra- and Intracellular Determinants of Tumor-Associated Macrophages as Tumor Promoters

Szebeni¹,

Vízler

Kitajka

et al. 2017

Mediators of Inflammation

171

145

View full text Add to dashboard Cite

One of the hallmarks of cancer-related inflammation is the recruitment of monocyte-macrophage lineage cells to the tumor microenvironment. These tumor infiltrating myeloid cells are educated by the tumor milieu, rich in cancer cells and stroma components, to exert functions such as promotion of tumor growth, immunosuppression, angiogenesis, and cancer cell dissemination. Our review highlights the ontogenetic diversity of tumor-associated macrophages (TAMs) and describes their main phenotypic markers. We cover fundamental molecular players in the tumor microenvironment including extra- (CCL2, CSF-1, CXCL12, IL-4, IL-13, semaphorins, WNT5A, and WNT7B) and intracellular signals. We discuss how these factors converge on intracellular determinants (STAT3, STAT6, STAT1, NF-κB, RORC1, and HIF-1α) of cell functions and drive the recruitment and polarization of TAMs. Since microRNAs (miRNAs) modulate macrophage polarization key miRNAs (miR-146a, miR-155, miR-125a, miR-511, and miR-223) are also discussed in the context of the inflammatory myeloid tumor compartment. Accumulating evidence suggests that high TAM infiltration correlates with disease progression and overall poor survival of cancer patients. Identification of molecular targets to develop new therapeutic interventions targeting these harmful tumor infiltrating myeloid cells is emerging nowadays.

show abstract

“…17 Based on in vitro observations, opposite CSF1-targeting strategies, such as recombinant CSF1 and CSF1 inhibitor, has been applied in a range of mice models and some cases of patients. [18][19][20][21][22] These therapeutics exhibit clinical benefits depending on types of cancer, adjuvant interventions and patient status, which bring more confusion to clinical applications of CSF1. The above observations suggest that a throughout investigation about CSF1 in tumor microenvironment is necessary, before CSF1-relevant strategies are applied in colon cancer.…”

Section: Introductionmentioning

confidence: 99%

Interactions between colon cancer cells and tumor-infiltrated macrophages depending on cancer cell-derived colony stimulating factor 1

et al. 2016

View full text Add to dashboard Cite

Tumor-infiltrated macrophages were potential targets of the immune therapy for patients with colon cancer. Colony stimulating factor 1 (CSF1) is a primary chemoattractant and functional regulator for macrophages, and therefore would be a feasible intervention for the macrophage-targeting therapeutics. However, the expression of CSF1 in colon cancer microenvironment and its roles in cancer development is largely unknown. In the present study, we found that CSF1 was over-expressed exclusively in colon cancer cells and was correlated with macrophages infiltration. The high CSF1 expression and macrophages infiltration were related to the tumor-node-metastasis (TNM) stage of colon cancer, and suggested to be positively associated with survival of colon cancer patients. In the studies based on an indirect Transwell system, we found that co-culture with macrophage promoted CSF1 production in colon cancer cells. Further investigation on regulatory mechanisms suggested that CSF1 production in colon cancer cells was dependent on PKC pathway, which was activated by IL-8, mainly produced by macrophages. Moreover, colon cancer cell-derived CSF1 drove the recruitment of macrophages and re-educated their secretion profile, including the augment of IL-8 production. The mice tumor xenografts study also found that over-expression of CSF1 in colon cancer cells promoted intratumoral infiltration of macrophages, and partially suppressed tumor growth. In all, our results demonstrated that CSF1 was an important factor in the colon cancer microenvironment, involving in the interactions between colon cancer cells and tumor-infiltrated macrophages.

show abstract

Delineating CSF-1-dependent regulation of myeloid cell diversity in tumors

Cited by 5 publications

References 10 publications

Roles of the immune system in cancer: from tumor initiation to metastatic progression

Roles of the immune system in cancer: from tumor initiation to metastatic progression

Inflammation and Cancer: Extra- and Intracellular Determinants of Tumor-Associated Macrophages as Tumor Promoters

Interactions between colon cancer cells and tumor-infiltrated macrophages depending on cancer cell-derived colony stimulating factor 1

Contact Info

Product

Resources

About