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doi:10.18632/oncotarget.v8i24

Cited by 6 publications

(4 citation statements)

References 5 publications

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“…Depletion of macrophages by blocking the CSF1/CSF1R axis in vivo has been demonstrated to reduce differentiation and survival of M2-type macrophages ( 68 ). Other drugs such as the BTKi ibrutinib also impacts the TME by exerting an immunomodulatory effect through regulation of tumour-infiltrating macrophages ( 69 ). In addition, ibrutinib downregulates PD-1 expression on T-cells, disrupts communication between MCL cells and macrophages, and impairs macrophage phagocytic function ( 70 ) ( Figure 1 ).…”

Section: Macrophages In MCL Therapymentioning

confidence: 99%

Empowering macrophages: the cancer fighters within the tumour microenvironment in mantle cell lymphoma

Nylund,

Nikkarinen,

et al. 2024

Front. Immunol.

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In Mantle Cell Lymphoma (MCL), the role of macrophages within the tumour microenvironment (TME) has recently gained attention due to their impact on prognosis and response to therapy. Despite their low absolute number in MCL tumour tissue, recent findings reveal an association between the levels of macrophages and prognosis, consistent with trends observed in other lymphoma subtypes. M2-like macrophages, identified by markers such as CD163, contribute to angiogenesis and suppression of the immune response. Clinical trials with MCL patients treated with chemoimmunotherapy and targeted treatments underscore the adverse impact of high levels of M2-like macrophages. Immunomodulatory drugs like lenalidomide reduce the levels of MCL-associated CD163+ macrophages and enhance macrophage phagocytic activity. Similarly, clinical approaches targeting the CD47 “don’t eat me” signalling, in combination with the anti-CD20-antibody rituximab, demonstrate increased macrophage activity and phagocytosis of MCL tumour cells. Cell-based therapies such as chimeric antigen receptor (CAR) T-cell have shown promise but various challenges persist, leading to a potential interest in CAR-macrophages (CAR-M). When macrophages are recruited to the TME, they offer advantages including phagocytic function and responsiveness to microenvironment alterations, suggesting their potential as a manipulable and inducible alternative when CAR T-cell therapies fails in the complex landscape of MCL treatment.

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Section: Macrophages In MCL Therapymentioning

confidence: 99%

Empowering macrophages: the cancer fighters within the tumour microenvironment in mantle cell lymphoma

Nylund,

Nikkarinen,

et al. 2024

Front. Immunol.

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“…CD25 is the α-chain of Interleukin-2 (IL-2) receptor expressed on the cell surface of Tregs and activated T effector cells. Transcription factor FOXP3 is crucial for the development, function, and lineage commitment of Tregs ( 7 , 10 ). It has been reported as a specific marker required for the development of thymic CD4 + CD25 + Tregs and is directly correlated with the cell surface expression of CD25 receptor ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

“…Treg family comprises of natural Tregs (nTregs) that express the nuclear forkhead or winged-helix family of transcription factor P3 (FoxP3), along with cell surface proteins cytotoxic T lymphocyte antigen-4 (CTLA-4) and CD25, as well as peripherally derived Tregs (pTregs) or those generated in vitro, known as induced Tregs (iTregs) (6). nTregs are characterized as CD4 + T cells expressing high levels of CD25 and FOXP3, and low levels of CD127 surface marker (7)(8)(9). CD25 is the a-chain of Interleukin-2 (IL-2) receptor expressed on the cell surface of Tregs and activated T effector cells.…”

Section: Introductionmentioning

confidence: 99%

Immune regulation and therapeutic application of T regulatory cells in liver diseases

Ajith,

Merimi,

Arki

et al. 2024

Front. Immunol.

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CD4+ CD25+ FOXP3+ T regulatory cells (Tregs) are a subset of the immunomodulatory cell population that can inhibit both innate and adaptive immunity by various regulatory mechanisms. In hepatic microenvironment, proliferation, plasticity, migration, and function of Tregs are interrelated to the remaining immune cells and their secreted cytokines and chemokines. In normal conditions, Tregs protect the liver from inflammatory and auto-immune responses, while disruption of this crosstalk between Tregs and other immune cells may result in the progression of chronic liver diseases and the development of hepatic malignancy. In this review, we analyze the deviance of this protective nature of Tregs in response to chronic inflammation and its involvement in inducing liver fibrosis, cirrhosis, and hepatocellular carcinoma. We will also provide a detailed emphasis on the relevance of Tregs as an effective immunotherapeutic option for autoimmune diseases, liver transplantation, and chronic liver diseases including liver cancer.

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“…[14][15][16] Similarly, lncRNAs, such as SChLAP1, 17 NEAT1, 18 and HOTTIP, 19 have been found to play critical roles in the development of PCa. Zinc finger antisense 1 (ZFAS1) is a member of lncRNA family associated with cancer, 20 and lncRNA ZFAS1 is reported to play a tumorigenic role in stomach cancer, 21 glioma, 22 nasopharyngeal carcinoma 23 and colorectal cancer. 24 At present, the specific role of ZFAS1 in PCa is not clear, the role of ZFAS1 has been recognized.…”

Section: Introductionmentioning

confidence: 99%

<p>lncRNA ZFAS1 Is Involved in the Proliferation, Invasion and Metastasis of Prostate Cancer Cells Through Competitively Binding to miR-135a-5p</p>

Pan¹,

Xu²,

Wang³

2020

CMAR

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Background: Prostate cancer (PCa) is a common malignant tumor in men. lncRNA ZFAS1 plays a carcinogenic role in many types of cancer; however, its potential role in PCa remains unclear. The current study aimed to determine the expression and function of ZFAS1 in PC. Methods: The ZFAS1 expression in PC tissues and cells was determined by quantitative polymerase chain reaction (qPCR). SiZFAS1, miR-135a-5p mimic and miR-135a-5p inhibitor were transfected into PCa cells. The direct target of ZFAS1 was predicted by Starbase and verified by dual-luciferase reporter. Cell viability, proliferation, apoptosis, migration and invasion of the PCa cells were determined by cell counting kit-8, clone formation assay, flow cytometer, scratch and Transwell assay, respectively. The expression levels of related proteins and mRNAs were determined by Western blotting and qPCR. Results: ZFAS1 expression was up-regulated in PCa cells and tissues. ZFAS1 could competitively bind to miR-135a-5p in PCa cells, and down-regulation of ZFAS1 inhibited cell viability, proliferation, migration, invasion of PCa cells and the occurrence of epithelial-mesenchymal transformation (EMT) and promoted apoptosis of PCa cells and increased the miR-135a-5p expression. Moreover, the function of miR-135a-5p mimic in PCa cells was consistent with ZFAS1 knockdown, while the function of miR-135a-5p inhibitor was opposite to that of miR-135a-5p mimic in PCa cells. The results showed that knocking down ZFAS1 could attenuate the effects of miR-135a-5p inhibitor on cell proliferation, invasion and EMT of PCa cells. Conclusion: Knocking down ZFAS1 could inhibit the proliferation, invasion and metastasis of PCa cells through regulating miR-135a-5p expression.

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Cited by 6 publications

References 5 publications

Empowering macrophages: the cancer fighters within the tumour microenvironment in mantle cell lymphoma

Empowering macrophages: the cancer fighters within the tumour microenvironment in mantle cell lymphoma

Immune regulation and therapeutic application of T regulatory cells in liver diseases

<p>lncRNA ZFAS1 Is Involved in the Proliferation, Invasion and Metastasis of Prostate Cancer Cells Through Competitively Binding to miR-135a-5p</p>

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