Опубликована: Янв. 1, 2024
Язык: Английский
Опубликована: Янв. 1, 2024
Язык: Английский
iScience, Год журнала: 2024, Номер 27(10), С. 110996 - 110996
Опубликована: Сен. 20, 2024
Язык: Английский
Процитировано
1Опубликована: Июнь 8, 2023
(1) Background: Breast cancer is a frequent heterogeneous disorder diagnosed in woman and high cause of mortality them reason to rapid metastasis disease recurrence. Ferroptosis can inhibit breast cell growth, improve the sensitivity chemotherapy radiotherapy distant metastases so potentially acts on tumor micro-environment; (2) Methods: Ferroptosis/Extracellular matrix remodeling literature text-mining results were integrated transcriptome cohort according their relapse free survival (DRFS) under adjuvant therapy (anthracyclin+taxanes) also MDA-MB-231 functional experiments with ferroptosis activations (GSE173905); (3) Results: identified 910 associated genes at list 10 articles. Univariate Cox analyses censored (GSE25066) selected 252 individual significant 171 found an adverse expression. Functional enrichment these predicted basal signatures. By some shared citations domain ECM such as: TNF, IL6, SET, CDKN2A, EGFR, HMGB1, KRAS, MET, LCN2, HIF1A, TLR4. A molecular score based expression eleven was predictive worst prognosis univariate level: subtype, short DRFS, grade values 3 4, estrogen progesterone receptors negative nodal stages 2 3. This gene signature validated as regulated by inductors (erastin RSL3) triple cellular model MDA-MB-231.; (4) Conclusions: Crosstalk between remodeling-Ferroptosis functionalities allowed define which have been characterized independent parameter patients. Gene this be erastin/RSL3 activators. could promising evaluate impact target therapies cancer.
Язык: Английский
Процитировано
2Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Янв. 23, 2024
Язык: Английский
Процитировано
0Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Янв. 25, 2024
Abstract Background The main reasons pancreatic cancer (PC) is difficult to treat are high tissue fibrosis and a strong immunosuppressive microenvironment. Therefore, it necessary elucidate the cause mechanism of tumour microenvironment formation. High-mobility group Box 1 (HMGB1) highly conserved nuclear protein that widely distributed in mammalian cells plays an important role tumours. However, functions mechanisms HMGB1 PC remain controversial. Here, we report novel for formation immune Methods In this study, expression level samples was detected patients TCGA database. relative serum tissues evaluated by enzyme-linked immunosorbent assay (ELISA). Flow cytometry used detect infiltration myeloid-derived suppressor (MDSCs) regulatory T tumours from xenograft mouse models treated with HMGB1. Vascular density cytokine levels were measured immunohistochemistry (IHC). HMGB1-associated differentially expressed genes GEPIA database analyse GO terms KEGG pathways. Subsequently, related proteins Western blotting. Results higher than normal tissues. High predict poor overall survival patients, suggesting its potential clinical significance prognosis. model results show significantly promotes growth. We further found CD69 + CD8 markedly decreased HMGB1-treated mice. Furthermore, after treatment HMGB1, into increased. IHC showed promoted intracellular inflammatory factors neovascularization. Mechanistically, indicated enhanced CXCL2 chemokines attract MDSCs upregulates through MAPK pathway. Conclusion conclusion, unexpected metastasis promoting microvessel mediated pathway recruit MDSC aggregation, which turn creates Thus, may be mediator therapeutic target regulating progression.
Язык: Английский
Процитировано
0Опубликована: Янв. 1, 2024
Язык: Английский
Процитировано
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