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Surufatinib increases cholangiocarcinoma cells radiosensitivity by anti-tumor proliferation and inhibition of macrophage M2 polarization

ABSTRACT: Surufatinib increases cholangiocarcinoma cells radiosensitivity by anti-tumor proliferation and inhibition of macrophage M2 polarization

PROVIDER: PRJNA1122142 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29344180_1.fastq.gz	Fastqsanger.gz
	SRR29344180_2.fastq.gz	Fastqsanger.gz
	SRR29344181_1.fastq.gz	Fastqsanger.gz
	SRR29344181_2.fastq.gz	Fastqsanger.gz
	SRR29344182_1.fastq.gz	Fastqsanger.gz

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Surufatinib increases cholangiocarcinoma cells radiosensitivity by anti-tumor proliferation and inhibition of macrophage M2 polarization

Project description:This study confirmed the radiosensitizing effects of surufatinib on cholangiocarcinoma. The mechanism is that surufatinib can activate TLR3, up-regulate the expression of TRIF protein, increase DNA damage and apoptosis after radiation, and up-regulate NF- κB signal pathway to inhibit M2 polarization of tumor-associated macrophages, thus enhance radiosensitivity.

2024-06-30 | GSE269494 | GEO

Immunoproteasome dysfunction augments alternative polarization of alveolar macrophages

Project description:The proteasome is a central regulatory hub for intracellular signaling by degrading numerous signaling mediators. Immunoproteasomes are specialized types of proteasomes known to be involved in shaping adaptive immune responses, but their role for innate immune signaling is elusive. Here, we analyzed immunoproteasome function for polarization of alveolar macrophages which are highly specialized tissue macrophages of the alveolar surface of the lung. Classical activation (M1 polarization) of primary alveolar macrophages by LPS/IFNÎ³ transcriptionally induced all three immunoproteasome subunits LMP2, LMP7, and MECL-1. In contrast, IL-4 triggered alternative (M2) activation was accompanied by posttranscriptional upregulation of LMP2 and LMP7. Accordingly, immunoproteasome activity increased in M1 cells, and to some extent under M2 conditions. Analyzing the polarization capability from LMP7 deficient mice revealed no effect on the LPS/IFNÎ³ triggered M1 profile, but uncovered a distorted M2 profile for IL-4 stimulated LMP7-/- alveolar macrophages as characterized by increased M2 marker gene expression and CCL17 cytokine release. This shift in immunoproteasome-dependent M2 polarization was accompanied by amplified AKT/STAT6 activation and IRF4 expression in LMP7-/- alveolar macrophages. IL-13 stimulation of LMP7 deficient cells induced a similar M2 skewed profile and IL4RÎ± protein expression was generally elevated in LMP7-/- alveolar macrophages, indicating that amplified IL4R signaling in immunoproteasome defective cells may contribute to augmented M2 polarization. Importantly, treatment with an LMP7-specific proteasome inhibitor recapitulated the findings of genetic LMP7 inactivation. Our results thus suggest a novel role of immunoproteasome function for regulating innate immune function of macrophages by limiting IL4R expression and signaling. Expression data of M0 and M2 macrophages derived from Lmp7 k.o. and control animals

2016-06-29 | E-GEOD-72000 | biostudies-arrayexpress

Expression data from macrophage maturation and polarization c-Myc in alternative macrophage activation experiments

Project description:In response to microenvironmental signals macrophages undergo different activation, indicated as classic/M1 and alternative/M2 polarization. C-Myc transcription factor could be an essential player in M2 polarization. Functional relevance of c-Myc in M2 macrophage biology is investigated by evaluating the effect of 100-58F4, on the transcriptional profile induced on human macrophages by IL-4. Human monocytes were obtained from normal donor buffy coats by two-step gradient centrifugation using Ficoll (Biochrom) and Percoll (Amersham). Non-adherent cells were discarded, and the purified monocytes were incubated for 7 days in RPMI 1640 (Biochom) supplemented with 10% FCS (HyClone) and 100 ng/mL M-CSF to obtain resting macrophages. Macrophage polarization was obtained by removing the culture medium and culturing cells in RPMI 1640 supplemented with 10% FCS and 100 ng/mL LPS plus 20 ng/mL IFN-gamma (M1 polarization) or 20 ng/mL IL-4 (M2 polarization) for 24 h. When needed, chemical inhibitors were added with IL-4.

2011-09-15 | E-GEOD-32164 | biostudies-arrayexpress

TIPE regulates TGFB2 expression and induces extracellular M2 polarization in CRC

Project description:Abstract Background: M2 macrophages (M2) play a crucial role in the development of colorectal cancer (CRC). The elevated expression of TIPE in CRC is closely associated with CRC progression; however, the impact of TIPE on M2 polarization remains unclear. Methods: IHC, WB, flow cytometry, qPCR, and IF were used to verify the promoting effect of TIPE on M2 polarization in specimens and in vitro co-culture models. RNA-seq, ELISA, and WB were used to identify the secreted proteins regulated by TIPE and the underlying mechanism. CCK-8 assay, wound healing assay, and transwell invasion assay were used to verify the effect of M2 on CRC. In vivo experiments were used to identify the promoting effect of TIPE on M2 polarization. Results: In this study, we first demonstrated that the abnormal overexpression of TIPE in CRC promotes M2 polarization and is correlated with a poor prognosis for CRC patients. We then found that TIPE activates the P38 MAPK signaling pathway in CRC to regulate TGFΒ2 secretion and, furthermore, induces M2 macrophage polarization. In subcutaneous and lung xenograft models of CRC in nude mice, we found that TIPE regulates TGFΒ2 secretion from human CRC to promote M2 polarization of murine macrophages. Conclusion: These results indicate that TIPE is a potent oncogene for inducing M2 polarization. It is suggested that all cancers with high TIPE expression need to be alert to the production and infiltration of M2 macrophages, which provides a new perspective for cancer treatment.

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Nab-paclitaxel induces DNA damage and inhibits M2 polarization of macrophages to achieve radiosensitization of cholangiocarcinoma cells.

Project description:Nab-paclitaxel induces DNA damage and inhibits M2 polarization of macrophages to achieve radiosensitization of cholangiocarcinoma cells.

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Identification of pharmacologic inhibitors and activators of IL-4-induced macrophage polarization

Project description:Macrophages polarize towards different subpopulations with distinct and partly antagonistic functions in various diseases. IFNγ/LPS-polarized M1-type macrophages can have antiangiogenic activity, whereas IL-4-induced M2-type macrophages can be proangiogenic and profibrotic. Therapeutic strategies to inhibit M2-type polarization while promoting M1-type polarization could serve to inhibit pathological angiogenesis and fibrosis. Here, by combining global quantitative time-course proteomics and phosphoproteomics with a small-molecule inhibitor screen we identify signaling events that promote specifically IL-4-induced and not IFNγ/LPS-induced macrophage polarization and found that the MEK inhibitor trametinib and the HDAC inhibitor panobinostat potently prevent M2-type macrophage polarization without inhibiting M1-type polarization. In contrast, selective B-Raf inhibition promotes M2-type polarization. Trametinib and panobinostat also blocked M2-type macrophage polarization and concomitantly angiogenesis and fibrosis in models of wound healing and neovascular age-related macular degeneration in vivo. Thus, these pharmacologic inhibitors could be utilized therapeutically to selectively block IL4-induced macrophage polarization and reduce pathologic angiogenesis and fibrosis.

2021-10-01 | GSE140235 | GEO

High-throughput integration of metabolic and transcriptional profiles reveals major metabolic regulators of macrophage polarization

Project description:Macrophages polarize to divergent functional phenotypes depending on their microenvironment in a highly coordinated process of metabolic and transcriptional rewiring that is still poorly understood. We developed an Integrated Metabolomics and Gene Expression (IMAGE) profiling and analysis pipeline and applied it to extensively characterize global metabolic programs of macrophage polarization. IMAGE analysis identified 7 major (novel and known) regulatory modules responsible for metabolic rewiring during polarization, which we validated through extensive carbon and nitrogen labeling experiments. M1-specific modules included: inflammatory variant of the aspartate-arginosuccinate shunt; TCA cycle break at Idh expression accompanied by citrate accumulation and production of itaconate and fatty acid synthesis. In M2 macrophages we discovered significant role of glutamine in polarization, providing nitrogen for UDP-GlcNAc synthesis. Consistently, glutamine deprivation results in significant M2-specific defect in polarization. Our data provide, for the first time, a global view of the integrated transcriptional and metabolic changes that result in M1 and M2 polarization. Bone-marrow derived macrophages were generated from C57BL/6 mice were plated at ~100k cells per well in 96-well plate and stimulated with either Il4 or combination of LPS&IFNg or left unstimulated for 24 h mRNA was derived from lysates using Invitrogen oligo-dT beads

2014-05-30 | E-GEOD-53053 | biostudies-arrayexpress

Identification of circular RNAs and mRNAs expression profiles in microglia M2 polarization [mRNA]

Project description:Microglia M2 polarization plays an important role in the regulation of neuroinflammation, but the molecular mechanisms behind it remain unclear. This study researched the expression profiles of mRNAs in microglia M2 polarization cell model.

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Identification of circular RNAs and mRNAs expression profiles in microglia M2 polarization [CircRNA]

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Identification of pharmacologic inhibitors and activators of IL-4-induced macrophage polarization [PBMC RNA-seq]

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