Time-Lapse 2D Imaging of Phagocytic Activity in M1 Macrophage-4T1 Mouse Mammary Carcinoma Cells in Co-cultures

Zaidi, Noorzaileen Eileena; Shazali, Nur Aima Hafiza; Leow, Adam Thean Chor; Osman, Mohamad; Ibrahim, Kamariah; Jaoi-Edward, Marilyn; Rahman, Nik Mohd Afizan Nik Abd

doi:10.3791/60281-v

Cited by 3 publications

(1 citation statement)

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“…Approximately 50% of the macrophage population has been detected in solid tumours and has been shown to perform an important pro-tumoral role [ 6 , 7 ]. Macrophages are heterogeneous and have a wide range of plasticity and functionality, allowing them to differentiate between separate phenotypes known as M1 (anti-tumoral phenotype) and M2 (pro-tumoral phenotype) depending on microenvironmental stimuli [ 8 , 9 ]. These macrophages are predominantly found infiltrated and differentiated within the TME and are known as “tumour-associated macrophages” or TAMs at all stages of tumour growth [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between Fatty Acid Metabolism and Tumour-Associated Macrophages in Cancer Progression

Zaidi¹,

Shazali²,

Leow³

et al. 2022

BioMedicine

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Summary Over the last few decades, cancer has been regarded as an independent and self sustaining progression. The earliest hallmarks of cancer comprise of sustaining proliferative signalling, avoiding growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Nonetheless, two emerging hallmarks are being described: aberrant metabolic pathways and evasion of immune destruction. Changes in tumour cell metabolism are not restricted to tumour cells alone; the products of the altered metabolism have a direct impact on the activity of immune cells inside the tumour microenvironment, particularly tumour-associated macrophages (TAMs). The complicated process of cancer growth is orchestrated by metabolic changes dictating the tight mutual connection between these cells. Here, we discuss approaches to exploit the interaction of cancer cells’ abnormal metabolic activity and TAMs. We also describe ways to exploit it by reprogramming fatty acid metabolism via TAMs.

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Section: Introductionmentioning

confidence: 99%

Crosstalk between Fatty Acid Metabolism and Tumour-Associated Macrophages in Cancer Progression

Zaidi¹,

Shazali²,

Leow³

et al. 2022

BioMedicine

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Targeting Innate Immunity in Cancer Therapy

et al. 2021

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The majority of current cancer immunotherapy strategies target and potentiate antitumor adaptive immune responses. Unfortunately, the efficacy of these treatments has been limited to a fraction of patients within a subset of tumor types, with an aggregate response rate of approximately 20% to date across all malignancies. The success of therapeutic inhibition of programmed death protein 1 (PD-1), protein death ligand 1 (PD-L1) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) with immune checkpoint inhibitors (ICI) has been limited to “hot” tumors characterized by preexisting T cell infiltration, whereas “cold” tumors, which lack T cell infiltration, have not achieved durable benefit. There are several mechanisms by which “cold” tumors fail to generate spontaneous immune infiltration, which converge upon the generation of an immunosuppressive tumor microenvironment (TME). The role of the innate immune system in tumor immunosurveillance and generation of antitumor immune responses has been long recognized. In recent years, novel strategies to target innate immunity in cancer therapy have emerged, including therapeutic stimulation of pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs); the DNA sensing cGAS/STING pathway; nucleotide-binding oligomerization domain-like receptors (NLRs), such as NLRP3; and the retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs). In addition, therapeutic modulation of key innate immune cell types, such as macrophages and natural killer cells, has been investigated. Herein, we review therapeutic approaches to activate innate immunity within the TME to enhance antitumor immune responses, with the goal of disease eradication in “cold” tumors. In addition, we discuss rational immune-oncology combination strategies that activate both innate and adaptive immunity, with the potential to enhance the efficacy of current immunotherapeutic approaches.

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Interleukin-27 Disrupts the Crosstalk of Apoptotic Activities between 4T1 Breast Cancer Cells and M2 Macrophages

Yusof¹,

Fuadi²,

Hamid³

et al. 2022

MJMHS

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Introduction: Cytokine immunotherapy such as Interleukin-27 (IL-27) has been foreseen as a promising alternative anti-cancer treatment. Thus, this study aimed to investigate whether IL-27 gene therapy regulates crosstalk between breast cancer cells and macrophages in the sense of pro-apoptotic activities. Methods: This study has led to the development of recombinant pcDNA3.4-IL27. The recombinant pcDNA3.4-IL27 was transfected into 4T1 murine mammary carcinoma cells alone and co-culture of 4T1 with M2 macrophages. The successful expression of IL-27 in the cells were determine through the immunofluorescence staining and detection of CD206, M2 macrophages marker. Apoptotic effects of pcDNA3.4-IL27 were assessed through MTT assay, Annexin V flow cytometer analysis, and AO/PI dual staining. Results: Our findings shows that pcDNA3.4-IL27 has the ability to induce apoptosis in both of the cell group and performs better in the co-culture of 4T1 with M2 macrophages compared to 4T1 cells alone. PcDNA3.4-IL27 induced apoptosis through the altered cell morphology and reduction in the number of viable cells. Conclusion: These data demonstrate that pcDNA3.4-IL27 has the ability to induce apoptosis in both 4T1 cell alone and co-cultured 4T1 with M2 macrophages. Thus, could serve as a potential anti cancer candidate against breast cancer.

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Time-Lapse 2D Imaging of Phagocytic Activity in M1 Macrophage-4T1 Mouse Mammary Carcinoma Cells in Co-cultures

Cited by 3 publications

References 0 publications

Crosstalk between Fatty Acid Metabolism and Tumour-Associated Macrophages in Cancer Progression

Crosstalk between Fatty Acid Metabolism and Tumour-Associated Macrophages in Cancer Progression

Targeting Innate Immunity in Cancer Therapy

Interleukin-27 Disrupts the Crosstalk of Apoptotic Activities between 4T1 Breast Cancer Cells and M2 Macrophages

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