Dataset Information

Proteomics based analysis for associated PD-L1 in macrophage stimulated with extracellular adenosine signaling

ABSTRACT: We performed proteomics analysis to discover effector proteins for the post-transcriptional regulation of PD-L1 onhuman macrophages stimulated by adenosine signal.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Primary Cell, Macrophage

DISEASE(S): Colon Cancer

SUBMITTER: Sang-Yeop Lee

LAB HEAD: Chang Hoon Lee

PROVIDER: PXD024512 | Pride | 2022-10-14

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	201123_KRICT_KCH_ADO_1st_01.raw	Raw
	201123_KRICT_KCH_ADO_1st_02.raw	Raw
	201123_KRICT_KCH_ADO_1st_03.raw	Raw
	201123_KRICT_KCH_ADO_1st_04.raw	Raw
	201123_KRICT_KCH_ADO_1st_05.raw	Raw

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Publications

Additive Effect of CD73 Inhibitor in Colorectal Cancer Treatment With CDK4/6 Inhibitor Through Regulation of PD-L1.

Noh Ji-Yoon JY Lee In Pyo IP Han Na Rae NR Kim Miok M Min Yong Ki YK Lee Sang-Yeop SY Yun Sung Ho SH Kim Seung Il SI Park Tamina T Chung Hyunmin H Park Daeui D Lee Chang Hoon CH

Cellular and molecular gastroenterology and hepatology 20220715 4

<h4>Background & aims</h4>Although cancer immunotherapies are effective for advanced-stage cancers, there are no clinically approved immunotherapies for colon cancers (CRCs). Therefore, there is a high demand for the development of novel therapies. Extracellular adenosine-mediated signaling is considered a promising target for advanced-stage cancers that are nonresponsive to programmed death 1 (PD-1)-/programmed death-ligand 1 (PD-L1)-targeted immunotherapies. In this study, we aimed to elucidat ...[more]

PMID: 35843546

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Project description:Background: Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide, most of which are caused by atherosclerosis. Discerning processes that participate in macrophage-to-foam cell formation are critical for understanding the basic mechanisms underlying atherosclerosis. To explore the molecular mechanisms of foam cell formation, the differentially expressed proteins were identified. Methods: In this paper, human monocytes, macrophage colony-stimulating factor induced macrophages, and oxidized low-density lipoprotein induced foam cells were cultured, and tandem mass tag (TMT) labeling combined with mass spectrometry (MS) were performed to find associations between foam cell transformation and proteome profiles. Results: Totally, 5146 quantifiable proteins were identified, among which 1515 and 182 differentially expressed proteins (DEPs) were found in macrophage/monocyte and foam cell/macrophage, respectively, using a cutoff of 1.5-fold change. Subcellular localization analysis revealed that downregulated DEPs of macrophages/monocytes were mostly located in the nucleus and upregulated DEPs of foam cells/macrophages mostly located in the plasma membrane and extracellular. Functional analysis of DEPs demonstrated that cholesterol metabolism related proteins were upregulated in foam cells, whereas the immune response-related proteins were downregulated in foam cells. The protein-interaction network showed that the DEPs with the highest interaction intensity between macrophages and foam cells were mainly concentrated in lysosomes and the endoplasmic reticulum. Conclusions: This study for the first time to perform quantitative proteomic investigation by TMT labeling and LC-MS/MS to identify differentially expressed proteins in human monocyte, macrophage, and foam cell. The results confirmed cholesterol metabolism was upregulated in foam cells, while immune response was suppressed, which suggested that foam cells were not the population that promote inflammation. In addition, KEGG enrichment analysis and protein-protein interaction indicated that the differentially expressed proteins locating in the endoplasmic reticulum and lysosomes may be key targets to regulate foam cell formation. These data provide a basis for identifying the potential proteins associated with the molecular mechanism involved in the transformation of macrophages to foam cells.