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Biology subjects

De Cecco, L.

Publications and source records attributed to De Cecco, L..

3 recordsLinked to original sources

ENPP3 expressed by HER2-positive breast cancer cells is associated with good prognosis by restraining epithelial-to-mesenchymal phenotype

Background Ectonucleotide pyrophosphatase/phosphodiesterase 3 (ENPP3/CD203c) is largely studied as a marker of mast cells and basophils. By depleting extracellular ATP, it prevents excessive activation of mast cells and basophils, hence reducing inflammation and allergic reactions. Recent findings have also shown that Enpp3 can deplete cGAMP, another molecule involved in STING activation and IFN-mediated pro-inflammation. Little is still known regarding the role of Enpp3 in non-immune cells although a few reports have described its expression in healthy tissues and tumors. Methods In silico analysis were performed to investigate the expression levels and the prognostic value of Enpp3 in breast cancer, together with ovarian, prostate and colon carcinoma. ENPP3 expression was evaluated in formalin-fixed, paraffin-embedded tumor samples of breast cancer patients by immunohistochemistry, and in mouse mammary cancer cell lines by western blots. Cells were treated with EGFR ligands to stimulate the EGFR/HER2 axis. A mouse-derived mammary cancer cell line was engineered by CRISPR/Cas9 to introduce a GFP sequence under the control of the Enpp3 promoter. GFP-positive and -negative cells were sorted and analyzed by gene expression profiling to identify genes and pathways associated with Enpp3 expression. Finally, wild type and Enpp3 knockout cells were injected in the fat pad of Wsh mice, which do not have mast cells, to evaluate the growth of the tumors which were further analyzed by immunohistochemistry. Results We provide evidence that HER2-positive cells express higher levels of ENPP3 in samples of breast cancer patients. Moreover, in vitro models confirmed that HER2 expression and EGFR stimulation result in up-regulation of Enpp3. We identified pathways that can concur to Enpp3 expression and showed that in vivo the absence of Enpp3 promotes tumor growth and development of tumors with a marked epithelial-to-mesenchymal phenotype. Finally, in a small cohort of HER2-positive breast cancer patients, we found that ENPP3 expression correlates with increased relapse-free survival. Conclusions Despite its potential immunosuppressive role, our findings support the notion that ENPP3 expression is promoted by HER2 in breast cancer, and that it is endowed with a positive prognostic value.

cancer biology↗

Active Surveillance Reveals a Systemic Pro-Resolving Th2 Immune Program Linked to 1 Desmoid Tumor Regression

Desmoid fibromatosis (DF) is a rare mesenchymal neoplasm with an unpredictable clinical course, where spontaneous regression or progression occurs in a significant subset of patients through largely undefined mechanisms. The use of active surveillance (AS) offers the opportunity to investigate whether tumor- or host-driven systemic and local immune features may explain these divergent outcomes, improving patient management. A prospective observational study enrolled 55 patients with primary sporadic DF managed with AS. Clinical evolution was categorized as progression, regression, or stable disease according to RECIST 1.1. Immunomonitoring with multicolor flow cytometry identified distinct systemic T-helper polarization states stratifying clinical trajectories: regressors showed a Th2-skewed profile, while progressors displayed activated T-helper cells and Th1/Th9/Th17 subsets. Higher baseline Th2 levels associated with regression and longer progression-free survival. Plasma proteomic and whole-blood transcriptomic analyses confirmed coordinated IL-4/IL-13-linked pro-resolving programs in regressors and inflammatory, early T-cell activation signatures in progressors. Tumor transcriptomics revealed adaptive, antigen-presentation and restrained immune programs in regressing lesions versus innate inflammatory, interferon and TGF-{beta}-driven fibrotic pathways in progressing tumors. These findings identify systemic T-helper polarization as a biomarker of DF behavior and highlight coordinated systemic-tumoral immune programs underlying clinical outcomes, supporting more precise clinical management.

immunology↗

SPARC regulation of PMN clearance protects from pristane induced lupus and rheumatoid arthritis

One step along the pathogenesis of Systemic lupus erythematosus (SLE) is associated with polymorphonuclear leukocyte (PMN) death and their ineffective removal by M2-macrophages. The secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein with unexpected immunosuppressive function in M2-macrophages and myeloid cells. To investigate the role of SPARC in autoimmunity, we adopted a pristane-induced model of lupus in mice, which recapitulates clinical manifestations of human SLE. Sparc-/- mice developed earlier and more severe renal disease, lung and liver parenchymal damage than the WT counterpart. Most prominently, Sparc-/- mice had anticipated and severe occurrence of arthritis. An intermediate phenotype was obtained in Sparc+/- hemizygous mice, a result that suggests Sparc gene-dosage as relevant in autoimmune-related events. Mechanistically, a defective Sparc expression in PMN blocks their clearance by macrophages, through a defective delivery of eat-me and dont eat-me signals. Sparc-/- PMN that escape macrophage scavenging becomes a source of autoantigens for dendritic cell (DC) presentation and a direct stimulus for IL-17 expression in {gamma}{delta}-T-cells. Gene profile analysis of synovial biopsies of knees affected by SLE-associated arthritis showed an inverse correlation between SPARC and key autoimmune genes. These results point to SPARC down-regulation as a key event characterizing SLE and associated rheumatoid arthritis pathogenesis.

immunology↗