Correlation between TAMs and proliferation and invasion of type I endometrial carcinoma

Hu, Honglin; Bai, Hansong; Pan, Haixia

doi:10.1016/j.apjtm.2015.07.009

Cited by 13 publications

(11 citation statements)

References 20 publications

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“…for the M2 TAMs dependence in the Estimated using Hu et al. ( 2015 ) cancer cell proliferation 0.05 Influx of the M2 TAMs Estimated 0.1 Inside tissue proliferation rate of M2 TAMs Estimated 2.4 Coeff. for the ECM stiffness dependence in the Estimated using Hayenga et al.…”

Section: Parameter Valuesmentioning

confidence: 99%

Directionality of Macrophages Movement in Tumour Invasion: A Multiscale Moving-Boundary Approach

2020

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Invasion of the surrounding tissue is one of the recognised hallmarks of cancer (Hanahan and Weinberg in Cell 100: 57–70, 2000. 10.1016/S0092-8674(00)81683-9), which is accomplished through a complex heterotypic multiscale dynamics involving tissue-scale random and directed movement of the population of both cancer cells and other accompanying cells (including here, the family of tumour-associated macrophages) as well as the emerging cell-scale activity of both the matrix-degrading enzymes and the rearrangement of the cell-scale constituents of the extracellular matrix (ECM) fibres. The involved processes include not only the presence of cell proliferation and cell adhesion (to other cells and to the extracellular matrix), but also the secretion of matrix-degrading enzymes. This is as a result of cancer cells as well as macrophages, which are one of the most abundant types of immune cells in the tumour micro-environment. In large tumours, these tumour-associated macrophages (TAMs) have a tumour-promoting phenotype, contributing to tumour proliferation and spread. In this paper, we extend a previous multiscale moving-boundary mathematical model for cancer invasion, by considering also the multiscale effects of TAMs, with special focus on the influence that their directional movement exerts on the overall tumour progression. Numerical investigation of this new model shows the importance of the interactions between pro-tumour TAMs and the fibrous ECM, highlighting the impact of the fibres on the spatial structure of solid tumour.

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Section: Parameter Valuesmentioning

confidence: 99%

Directionality of Macrophages Movement in Tumour Invasion: A Multiscale Moving-Boundary Approach

2020

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“…TAMs regulate tumorigenesis, development and metastasis in a variety of ways (3,4). The proliferation of TAMs and the secretion of inflammatory factors have promoted the development of type I EC (5). The density of TAMs in type II endometrial carcinoma is almost twice that of type I EC, and this difference may be due to the predominant result of M1 macrophages in the type II EC (6).…”

Section: Introductionmentioning

confidence: 99%

Colony‑stimulating factor 1 receptor inhibition blocks macrophage infiltration and endometrial cancer cell proliferation

Tian

Gao

et al. 2019

Mol Med Report

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Tumor-associated macrophages (TAMs) promote the progression of endometrial cancer (EC), but the mechanism of TAM in EC cell proliferation remains unclear. It was found that colony stimulating factor (CSF)-1 and CSF-1 receptor (CSF-1R) were highly expressed in EC tissues of patients and two EC cell lines (ECC-1 and HEC-1A). Using wound-healing and chemotactic migration assays to evaluate the role of EC cells in the induction of macrophage migration, it was found that the supernatant of EC cells promoted macrophage cell line (U937) migration; however, the migration capacity of U937 weakened when CSF-1R was blocked. Subsequently, inhibition of CSF-1 expression in EC cells also restrained U937 migration. Additionally, blocking CSF-1R by PLX3397 treatment in U937 cells inhibited EC cell proliferation in a co-culture system by inhibiting the expression of proliferation-associated proteins (Janus kinase-1, phosphoinositide 3-kinase, AKT, cyclin kinase 2, 4 and retinoblastoma-associated protein). Together, these results demonstrated that CSF-1 secreted by EC cells promoted macrophage migration; similarly, CSF-1-stimulated macrophages promoted EC cell proliferation. These results suggested that the interaction between CSF-1 and its receptor served an important role in promoting macrophage infiltration and progression of EC.

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“…On the one hand, similar to both TAMs populations, we consider the proliferation effect-function p (σ ) defined in Equation ( 4) to explore the influence of the available nutrients on the rate of cancer cell proliferation. On the other hand, biological evidence shows that while M2 TAMs promote cancer cell proliferation [67], M1 TAMs inhibits this [68]. Thus, expanding here the proliferation law introduced in Suveges et al [30] by accounting for the negative effect of M1 TAMs, we obtain leading to the following proliferation law:…”

Section: Dynamics Of the Cancer Cell Populationmentioning

confidence: 59%

Re-polarisation of Macrophages Within Collective Tumour Cell Migration: A Multiscale Moving Boundary Approach

Suveges

Eftimie

Trucu

2022

Front. Appl. Math. Stat.

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Cancer invasion of the surrounding tissue is a multiscale process of collective cell movement that involves not only tumour cells but also other immune cells in the environment, such as the tumour-associated macrophages (TAMs). The heterogeneity of these immune cells, with the two extremes being the pro-inflammatory and anti-tumour M1 cells, and the anti-inflammatory and pro-tumour M2 cells, has a significant impact on cancer invasion as these cells interact in different ways with the tumour cells and with the ExtraCellular Matrix (ECM). Experimental studies have shown that cancer cells co-migrate with TAMs, but the impact of these different TAM sub-populations (which can change their phenotype and re-polarise depending on the microenvironment) on this co-migration is not fully understood. In this study, we extend a previous multi-scale moving boundary mathematical model, by introducing the M1-like macrophages alongside with their exerted multi-scale effects on the tumour invasion process. With the help of this model we investigate numerically the impact of re-polarising the M2 TAMs into the anti-tumoral M1 phenotype and how such a strategy affects the overall tumour progression. In particular, we investigate numerically whether the M2→M1 re-polarisation could depend on time and/or space, and what would be the macroscopic effects of this spatial- and temporal-dependent re-polarisation on tumour invasion.

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Correlation between TAMs and proliferation and invasion of type I endometrial carcinoma

Abstract: Increase of the number of infiltrating macrophages and its contribution to the tumor inflammatory microenvironment may result in the development of the type I endometrial carcinoma.

Cited by 13 publications

References 20 publications

Directionality of Macrophages Movement in Tumour Invasion: A Multiscale Moving-Boundary Approach

Directionality of Macrophages Movement in Tumour Invasion: A Multiscale Moving-Boundary Approach

Colony‑stimulating factor 1 receptor inhibition blocks macrophage infiltration and endometrial cancer cell proliferation

Re-polarisation of Macrophages Within Collective Tumour Cell Migration: A Multiscale Moving Boundary Approach

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