ANXA1 Contained in EVs Regulates Macrophage Polarization in Tumor Microenvironment and Promotes Pancreatic Cancer Progression and Metastasis

Novizio, Nunzia; Belvedere, Raffaella; Pessolano, Emanuela; Morello, Silvana; Tosco, Alessandra; Campiglia, Pietro; Filippelli, Amelia; Petrella, Antonello

doi:10.3390/ijms222011018

Cited by 31 publications

(20 citation statements)

References 65 publications

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“…ANXA1-containing extracellular vesicles also regulate macrophage polarization in the TIME and promote the development and metastasis of pancreatic cancer. And the typical immunostaining graphs of three genes in BLCA tumor tissue were provided by the human protein atlas (HPA) database (Supplementary Figure S5) (Novizio et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Using Necroptosis-Associated Genes To Predict The Immune Microenvironment And Prognosis Of Bladder Urothelial Carcinoma

Liu

Yang

et al. 2022

Preprint

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PURPOSE Bladder urothelial carcinoma (BLCA), the most common urinary tract malignancy, has a high recurrence rate and poor survival at late stages. Necroptosis, a form of programmed cell death, is involved in cancer development and progression, but its function in BLCA prognosis remains unclear. This study sought to investigate the role of necroptosis in the development and prognosis of BLCA. METHODS Clinical information and RNA expression matrix data were obtained from the databases. Survival analysis was performed to obtain survival- and necroptosis-related genes and identify any that overlapped. Consensus clustering analysis was used to create different subgroups by combining the overlapping gene expression matrix and clinical information. The tumor immune microenvironment and immune status of the different subgroups were determined using ESTIMATE, MCPcounter, and ssGSEA analysis. We performed differential analysis on the gene expression matrix of molecular subpopulations to find and screen out differentially expressed genes (DEGs). GO, KEGG, GSVA, and GSEA analyses were used to elucidate the underlying mechanisms of the DEGs. Lasso Cox regression analysis was used to build a prognostic risk model and perform a pan-cancer analysis of the screened genes. The results were used to define potential roles for these genes in other cancers and assess the efficacy of the risk model. RESULTS Cluster analysis identified two subgroups, C1 and C2, with significantly different survival rates. ESTIMATE, MCPcounter, and ssGSEA analyses showed that high immune scores, tumor purity, and immune status were associated with poorer prognoses. GO and KEGG functional enrichment analyses indicated that DEGs were mainly focused on tumor proliferation, invasion, and immunity and GSEA analysis suggested that necroptosis may affect Toll-like receptor signaling pathways, MAPK cascade regulation of leukocyte trafficking, and cytokine-cytokine receptor interaction pathways. Lasso Cox regression analysis was used to model the prognostic risk while screening for representative necroptosis-associated genes, ANXA1, ATAD3A, and TRPC6, with high potential for survival prediction in BLCA patients. The pan-cancer analysis indicated that the three representative genes were also differentially expressed in other cancer types. CONCLUSION Expression of necroptosis-related genes such as ANXA1, ATAD3A, and TRPC6 correlate with the immune microenvironment of BLCA patients and have the potential for use in disease prognostics.

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Section: Discussionmentioning

confidence: 99%

Using Necroptosis-Associated Genes To Predict The Immune Microenvironment And Prognosis Of Bladder Urothelial Carcinoma

Liu

Yang

et al. 2022

Preprint

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“…The clonogenic potential [ 52 ] was assessed using a subtoxic dose (20 μM) of the 6-OHDA and fraction III 6 µg/mL. Cells were plated in 6-well plates at a seeding density of 2 × 10 3 cells/well.…”

Section: Methodsmentioning

confidence: 99%

Cocoa Extract Provides Protection against 6-OHDA Toxicity in SH-SY5Y Dopaminergic Neurons by Targeting PERK

et al. 2022

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Parkinson’s disease (PD) represents one of the most common neurodegenerative disorders, characterized by a dopamine (DA) deficiency in striatal synapses and misfolded toxic α-synuclein aggregates with concomitant cytotoxicity. In this regard, the misfolded proteins accumulation in neurodegenerative disorders induces a remarkable perturbations of endoplasmic reticulum (ER) homeostasis leading to persistent ER stress, which in turn, effects protein synthesis, modification, and folding quality control. A large body of evidence suggests that natural products target the ER stress signaling pathway, exerting a potential action in cancers, diabetes, cardiovascular and neurodegenerative diseases. This study aims to assess the neuroprotective effect of cocoa extract and its purified fractions against a cellular model of Parkinson’s disease represented by 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y human neuroblastoma. Our findings demonstrate, for the first time, the ability of cocoa to specifically targets PERK sensor, with significant antioxidant and antiapoptotic activities as both crude and fractioning extracts. In addition, cocoa also showed antiapoptotic properties in 3D cell model and a notable ability to inhibit the accumulation of α-synuclein in 6-OHDA-induced cells. Overall, these results indicate that cocoa exerts neuroprotective effects suggesting a novel possible strategy to prevent or, at least, mitigate neurodegenerative disorders, such as PD.

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“…Neutralizing annexin 1 with an n‐terminal antibody and gene silencing attenuated EV tethering and the capacity for 3D acellular collagen hydrogen microcalcification formation. Linking this phenomenon to inflammation, it has recently been postulated that EVs that contain annexin 1 may also regulate macrophage polarization, 68 however, further investigation into this is currently underway.…”

Section: Extracellular Vesicles Are “Hidden” Calcific Initiators and ...mentioning

confidence: 99%

Small particles with large impact: Insights into the unresolved roles of innate immunity in extracellular vesicle‐mediated cardiovascular calcification

Turner

Bartoli-Leonard

Aikawa

2022

Immunological Reviews

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Summary Extracellular vesicles (EVs) are critical in the initiation and progression of cardiovascular calcification, and immune cell infiltration and inflammation have a central role in this process. EVs egress from various cardiovascular cell types, which when acquiring specific properties, become calcifying. These calcifying EVs form nidi for microcalcification, which can progress to the macrocalcification lesions that are visualized clinically. We make the distinction between inflammatory‐driven and mineral dysregulation‐driven calcification, which both share EVs as a central initiator. In inflammation‐mediated calcification, inflammation precedes microcalcification and results from EV release from macrophages. Local cellular crosstalk mediated by EVs as well as circulating EVs and other inflammatory nanoparticles, such as calciprotein particles and lipoproteins, are also critical in the progression of cardiovascular calcification. It is imperative that future work links the already established and to be discovered roles of inflammation and innate immunity in cardiovascular calcification to these key signaling and functional roles of these nanoparticles. It remains an understudied area with high potential to unravel mechanistic roles and has important implications in drug target research.

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ANXA1 Contained in EVs Regulates Macrophage Polarization in Tumor Microenvironment and Promotes Pancreatic Cancer Progression and Metastasis

Cited by 31 publications

References 65 publications

Using Necroptosis-Associated Genes To Predict The Immune Microenvironment And Prognosis Of Bladder Urothelial Carcinoma

Using Necroptosis-Associated Genes To Predict The Immune Microenvironment And Prognosis Of Bladder Urothelial Carcinoma

Cocoa Extract Provides Protection against 6-OHDA Toxicity in SH-SY5Y Dopaminergic Neurons by Targeting PERK

Small particles with large impact: Insights into the unresolved roles of innate immunity in extracellular vesicle‐mediated cardiovascular calcification

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