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Transcriptomic profiling of macrophage induced breast cancer cells

ABSTRACT: Transcriptomic profiling of macrophage induced breast cancer cells

PROVIDER: PRJNA872180 | ENA |

REPOSITORIES: ENA

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Transcriptomic profiling of macrophage induced breast cancer cells

Project description:To infestigate the effect of macrophage on breast cancer cells, we treated breast cancer cells with medium from either monocyte derived macrophages or breast cancer cell medium treated monocyte derived macrophages

2022-11-14 | GSE211821 | GEO

Transcriptomic analysis of control and macrophage-conditioned meduim treated MCF-7 breast cancer cells to investigate the mechanism of macrophage-induced TNT formation.

Project description:Transcriptomic analysis of control and macrophage-conditioned meduim treated MCF-7 breast cancer cells to investigate the mechanism of macrophage-induced TNT formation.

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Transcriptomic analysis of control and macrophage-conditioned meduim treated MCF-7 breast cancer cells to investigate the mechanism of macrophage-induced TNT formation.

Project description:Tumor-associated macrophages (TAMs) secrete cytokines, chemokines, and growth factors in tumor microenvironment to support cancer progression. Previous studies have demonstrated role of macrophages in stimulating long range intercellular bridges referred as tunneling nanotubes (TNTs) in cancer cells. Intercellular communication between cancer cells via TNTs promote cancer growth, invasion, and therapy resistance. Given the important role of TNTs and macrophages in cancer, the mechanism of macrophage mediated TNT formation is elusive. In this study, it is shown that the macrophage-conditioned medium treated MCF-7 cells showed enrichment of NFκB and focal adhesion pathway as well as upregulation of genes involved in EMT, extracellular remodelling, and actin cytoskeleton reorganization. Interestingly, inhibition of PKC, Src, NFκB and p38 inhibited macrophage-induced TNT formation in MCF-7 cells. These results reveal novel role of PKC and Src in inducing TNT formation in cancer cells and suggest that inhibition of PKC and Src activity may likely contribute to reduced macrophage-breast cancer cell interaction and potential therapeutic strategy of cancer.

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Transcriptomic sequencing of breast cancer

Project description:Transcriptomic sequencing of breast cancer

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Zeb1-induced metabolic reprogramming of glycolysis is essential for macrophage polarization in breast cancer

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Transcriptomic analysis of breast cancer

Project description:Transcriptomic analysis of fresh breast cancer tissue versus normal tissues. The Study comprising 45 Saudi-Arabian subjects was designed to take advantage of transcriptomics to prospectively explore the roles of lifestyle and genetic susceptibility in the occurrence of breast cancer. Total RNA isolated from 45 surgically resected breast cancer tissues and 8 healthy breast tissues (3 from Affymetrix) and purified, labeled, and hybridized to Affymetrix Human Gene 1.0 ST Array.

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Transcriptomic profiling of breast cancer cells incubated in vitro with surgical wound fluids from patients with breast cancer

Project description:Transcriptomic profiling of breast cancer cells incubated in vitro with surgical wound fluids from patients with breast cancer reveals similarities in the biological response induced by intraoperative radiation therapy and the radiation-induced bystander effect In patients with breast cancer who undergo breast-conserving surgery (BCS), more than 90% of local recurrences occur in the same quadrant as the primary cancer. Surgical wound fluids (SWF) are believed to play a role in this process by inducing an inflammatory process in the scar tissue area. Despite strong clinical data demonstrating the benefits of intraoperative radiotherapy (IORT), the biological basis underlying this process remains poorly understood. Ionizing radiation (IR) directly affects cells by damaging DNA, thereby altering the cell phenotype. IR direct effects cancer cells and also influences unirradiated cells located nearby, a phenomenon known as the radiation-induced bystander effect (RIBE), significantly modifying the tumour microenvironment. We hypothesized that SWF obtained from patients after breast-conserving surgery (BCS) and IORT would induce a radiobiological response (due to RIBE) in unirradiated cells, thereby modifying their phenotype.

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Mouse modeling dissecting macrophage-breast cancer communication uncovered roles of PYK2 in macrophage recruitment and breast tumorigenesis

Project description:Mouse modeling dissecting macrophage-breast cancer communication uncovered roles of PYK2 in macrophage recruitment and breast tumorigenesis

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Mouse modeling dissecting macrophage-breast cancer communication uncovered roles of PYK2 in macrophage recruitment and breast tumorigenesis

Project description:Macrophage infiltration in mammary tumors is associated with enhanced tumor progression, metastasis, and poor clinical outcome, and considered as target for therapeutic intervention. Here we used different genetic mouse models and show that ablation of the tyrosine kinase PYK2, either in breast cancer cells, only in the tumor microenvironment, or both, markedly reduced the number of infiltrating tumor macrophages and concomitantly inhibited tumor angiogenesis and tumor growth. Strikingly, PYK2 depletion only in macrophages was sufficient to induce similar effects. These phenotypic changes were associated with reduced monocyte recruitment and a substantial decrease in tumor-associated macrophages (TAMs). Mechanistically, we show that PYK2 mediates mutual communication between breast cancer cells and macrophages through critical effects on key receptor signaling. Specifically, PYK2 ablation inhibited Notch1 signaling and consequently reduced CCL2 secretion by breast cancer cells, and concurrently reduced the levels of CCR2, CXCR4, IL4R, and Stat6 activation in macrophages. These bidirectional effects modulate monocyte recruitment, macrophage polarization and tumor angiogenesis. PYK2 expression is correlated with infiltrated macrophages in breast cancer patients, and its significant effects on macrophage infiltration and their pro-tumorigenic phenotype suggest that PYK2 targeting can be utilized as an effective strategy to modulate TAMs and possibly sensitize breast cancer to immunotherapy.

2022-02-09 | GSE193168 | GEO

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