M1 Macrophages Enhance Survival and Invasion of Oral Squamous Cell Carcinoma by Inducing GDF15-Mediated ErbB2 Phosphorylation

Lv, Chunxu; Li, Shutong; Zhao, Jingjing; Yang, Pishan; Yang, Chengzhe

doi:10.1021/acsomega.2c00571

Cited by 24 publications

(18 citation statements)

References 40 publications

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“…However, several studies reached opposite conclusions. For example, M2 macrophages may have a partial limiting effect on colorectal cancer metastasis ( 62 ), whereas M1 macrophages promote tumor progression ( 63 , 64 ). Therefore, the characteristics of TAMs contribute to better understanding the cancer states and exploring new ways to block or eradicate cancers.…”

Section: Macrophages Regulate Tumor Progressionmentioning

confidence: 99%

The role of macrophages-mediated communications among cell compositions of tumor microenvironment in cancer progression

Jiang

Wei

et al. 2023

Front. Immunol.

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Recent studies have revealed that tumor-associated macrophages are the most abundant stromal cells in the tumor microenvironment and play an important role in tumor initiation and progression. Furthermore, the proportion of macrophages in the tumor microenvironment is associated with the prognosis of patients with cancer. Tumor-associated macrophages can polarize into anti-tumorigenic phenotype (M1) and pro-tumorigenic phenotype (M2) by the stimulation of T-helper 1 and T-helper 2 cells respectively, and then exert opposite effects on tumor progression. Besides, there also is wide communication between tumor-associated macrophages and other immune compositions, such as cytotoxic T cells, regulatory T cells, cancer-associated fibroblasts, neutrophils and so on. Furthermore, the crosstalk between tumor-associated macrophages and other immune cells greatly influences tumor development and treatment outcomes. Notably, many functional molecules and signaling pathways have been found to participate in the interactions between tumor-associated macrophages and other immune cells and can be targeted to regulate tumor progression. Therefore, regulating these interactions and CAR-M therapy are considered to be novel immunotherapeutic pathways for the treatment of malignant tumors. In this review, we summarized the interactions between tumor-associated macrophages and other immune compositions in the tumor microenvironment and the underlying molecular mechanisms and analyzed the possibility to block or eradicate cancer by regulating tumor-associated macrophage-related tumor immune microenvironment.

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Section: Macrophages Regulate Tumor Progressionmentioning

confidence: 99%

The role of macrophages-mediated communications among cell compositions of tumor microenvironment in cancer progression

Jiang

Wei

et al. 2023

Front. Immunol.

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“…In most of the peripheral tissues such as the kidney, the GDF15 receptor GFRAL is absent, 53 indicating that the peripheral action of this factor must be transduced by another receptor. Whether GDF15 directly binds to ErbB2 receptor remains to be established, however, it is involved in the activation of this receptor in different types of cancer [54][55][56] where it promotes cell proliferation and pErbB2 was successfully immunoprecipitated with GDF15. 57 The consequences of this inadaptation are a loss of K + in the urine and a rapid decrease in the plasma K + level, indicating that GDF15-mediated AIC proliferation is of major importance in response to K + restriction.…”

Section: A Gdf15-erbb2-hka2 Axis Contributing To Aic Proliferationmentioning

confidence: 99%

GDF15 mediates renal cell plasticity in response to potassium depletion in mice

Lasaad,

Walter,

Rafael

et al. 2023

Acta Physiologica

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ObjectiveTo understand the mechanisms involved in the response to a low‐K+ diet (LK), we investigated the role of the growth factor GDF15 and the ion pump H,K‐ATPase type 2 (HKA2) in this process.MethodsMale mice of different genotypes (WT, GDF15‐KO, and HKA2‐KO) were fed an LK diet for different periods of time. We analyzed GDF15 levels, metabolic and physiological parameters, and the cellular composition of collecting ducts.ResultsMice fed an LK diet showed a 2–4‐fold increase in plasma and urine GDF15 levels. Compared to WT mice, GDF15‐KO mice rapidly developed hypokalemia due to impaired renal adaptation. This is related to their 1/ inability to increase the number of type A intercalated cells (AIC) and 2/ absence of upregulation of H,K‐ATPase type 2 (HKA2), the two processes responsible for K+ retention. Interestingly, we showed that the GDF15‐mediated proliferative effect on AIC was dependent on the ErbB2 receptor and required the presence of HKA2. Finally, renal leakage of K+ induced a reduction in muscle mass in GDF15‐KO mice fed LK diet.ConclusionsIn this study, we showed that GDF15 and HKA2 are linked and play a central role in the response to K+ restriction by orchestrating the modification of the cellular composition of the collecting duct.

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“…In most of the peripheral tissues such as kidneys, the GDF15 receptor GFRAL is absent (42), indicating that the peripheral action of this factor must be transduced by another receptor. Whether GDF15 directly binds to ErbB2 receptor remains to be clearly establish, however, it has already been involved in the activation of this receptors in different types of cancer (43)(44)(45) where it promotes cell proliferation and pErbB2 was successfully immunoprecipitated with GDF15 (46). The consequences of this inadaptation are a loss of K + in the urine and a rapid decrease of the plasma K + level, indicating that GDF15-mediated AIC proliferation is of major importance in response to K + restriction.…”

Section: Gdf15 Regulates Renal Ion Excretionmentioning

confidence: 99%

GDF15 mediates renal cell plasticity in response to potassium depletion

Lasaad

Walter

Rafael

et al. 2022

Preprint

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A low potassium (K+) intake is a common situation in the population of the Westernized countries where processed food is prevalent in the diet. Here, we show that expression of GDF15, a TGFbeta-related growth factor, is increased in renal tubular segments and gut parts of mice in response to low-K+ diet leading to a systemic elevation of its plasma and urine concentration. In human, under mild dietary K+ restriction, we observed that urine GDF15 excretion is correlated with plasma K+ level. Conversely to WT mice, adaptation to K+ restriction of GDF15-KO mice is not optimal, they do not increase their number of type A intercalated cell, responsible for K+ retention, and have a delayed renal K+ retention, leading to early development of hypokalemia. This renal effect of GDF15 depends on ErBb2 receptor, whose expression is increased in the kidney collecting ducts. We also observe that, in the absence of GDF15, the release of K+ by the muscles is blunted which is compensated by a loss of muscle mass. Thus, in this study, we showed that GDF15 plays a central role in the response to K+ restriction by orchestrating the modification of the cell composition of the collecting duct.

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M1 Macrophages Enhance Survival and Invasion of Oral Squamous Cell Carcinoma by Inducing GDF15-Mediated ErbB2 Phosphorylation

Cited by 24 publications

References 40 publications

The role of macrophages-mediated communications among cell compositions of tumor microenvironment in cancer progression

The role of macrophages-mediated communications among cell compositions of tumor microenvironment in cancer progression

GDF15 mediates renal cell plasticity in response to potassium depletion in mice

GDF15 mediates renal cell plasticity in response to potassium depletion

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