CD47 Contributes to the Proliferation of Breast Cancer DOI Creative Commons

Junbin Wang,

Xia Wu,

Xuejian Liu

и другие.

Frontiers in Bioscience-Landmark, Год журнала: 2025, Номер 30(3)

Опубликована: Март 5, 2025

Background: The CD47 molecule (CD47) performs a novel role in regulating immunoreactions by binding to signal-regulatory protein alpha (SIRPα), resulting the tumorigenesis of multiple malignant neoplasms. However, its effects and mechanisms breast cancer (BC) remain unknown. Methods: To explore molecular explicit impacts CD47, we screened two databases for CD47-associated signaling pathways cellular functions. BC samples patients’ basic information were collected identify statistical significance expression. We also constructed experiments validate regulatory cell proliferation. Results: Analysis TCGA-BRCA, GSE42568, GSE15852 datasets demonstrated an elevated level tissues. A Venn diagram revealed 11,194 co-expressed genes, pathway analysis linked levels critical pathways, such as cytokine-receptor interactions Janus kinase/signal transducer activator transcription (JAK/STAT) signaling, which are integral proliferation invasiveness. Clinical data from 108 specimens showed that localization was primarily membranous, with higher correlating marker Ki-67 (Ki-67) expression (p < 0.0001) advanced tumor/node/metastasis (TNM) stage 0.0001). Additionally, functional assays depletion reduced viability 0.01), migration 0.001), invasion 0.05 4T1 cells; p 0.001 MDA-MB-231 cells) vitro led smaller tumor volumes vivo. Conclusion: is key regulator invasiveness serves potential assessing aggressiveness guiding therapeutic strategies.

Язык: Английский

Metabolic reprogramming and therapeutic resistance in primary and metastatic breast cancer DOI Creative Commons
Shan Liu,

Xingda Zhang,

Wenzheng Wang

и другие.

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Ноя. 21, 2024

Metabolic alterations, a hallmark of cancer, enable tumor cells to adapt their environment by modulating glucose, lipid, and amino acid metabolism, which fuels rapid growth contributes treatment resistance. In primary breast metabolic shifts such as the Warburg effect enhanced lipid synthesis are closely linked chemotherapy failure. Similarly, metastatic lesions often display distinct profiles that not only sustain but also confer resistance targeted therapies immunotherapies. The review emphasizes two major aspects: mechanisms driving in both how unique environments sites further complicate treatment. By targeting vulnerabilities at stages, new strategies could improve efficacy existing provide better outcomes for cancer patients.

Язык: Английский

Процитировано

16

Myeloid cell-derived apCAFs promote HNSCC progression by regulating proportion of CD4+ and CD8+ T cells DOI Creative Commons

Feilong Ren,

Lin Meng,

Shize Zheng

и другие.

Journal of Experimental & Clinical Cancer Research, Год журнала: 2025, Номер 44(1)

Опубликована: Янв. 31, 2025

Язык: Английский

Процитировано

2

Oral Cancer Stem Cells: A Comprehensive Review of Key Drivers of Treatment Resistance and Tumor Recurrence DOI

P. J. Nagarathna,

Santosh Patil, Vishnu Priya Veeraraghavan

и другие.

European Journal of Pharmacology, Год журнала: 2025, Номер unknown, С. 177222 - 177222

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

1

Golgi protein 73: the driver of inflammation in the immune and tumor microenvironment DOI Creative Commons

Pingping Feng,

Xinyang Hu, Sining Zhou

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 15

Опубликована: Янв. 8, 2025

Golgi Protein 73 (GP73) is a Golgi-resident protein that highly expressed in primary tumor tissues. Initially identified as an oncoprotein, GP73 has been shown to promote development, particularly by mediating the transport of proteins related epithelial-mesenchymal transition (EMT), thus facilitating cell EMT. Though our previous review summarized functional roles intracellular signal transduction and its various mechanisms promoting EMT, recent studies have revealed plays crucial role regulating immune microenvironment. can modulate signaling pathways influence cytokine chemokine networks, resulting inflammation caused viral bacterial infection or diseases, leading microenvironment deteriorated. Additionally, extracellular also regulate target cells binding their cell-surface receptors entering acceptor cells, thereby development. In this review, we aim summarize findings, providing insights for future investigations on potential therapeutic ameliorating chronic

Язык: Английский

Процитировано

1

Molecular Insights on Signaling Cascades in Breast Cancer: A Comprehensive Review DOI Open Access
Venketesh K. Panda,

Barnalee Mishra,

Samikshya Mahapatra

и другие.

Cancers, Год журнала: 2025, Номер 17(2), С. 234 - 234

Опубликована: Янв. 13, 2025

The complex signaling network within the breast tumor microenvironment is crucial for its growth, metastasis, angiogenesis, therapy escape, stem cell maintenance, and immunomodulation. An array of secretory factors their receptors activate downstream cascades regulating cancer progression metastasis. Among various pathways, EGFR, ER, Notch, Hedgehog pathways have recently been identified as in terms proliferation, survival, differentiation, maintenance CSCs, failure. These mediate such MAPK, including MEK/ERK that promote common pro-oncogenic signaling, whereas dysregulation PI3K/Akt, Wnt/β-catenin, JAK/STAT activates key oncogenic events drug resistance, CSC enrichment, metabolic reprogramming. Additionally, these orchestrate an intricate interplay between stromal cells, immune cells. Metabolic reprogramming adaptations contribute to aggressive are unresponsive therapy. Herein, recent insights into novel operating TME aid advancement emphasized current developments practices targeting enhance treatment efficacy reviewed.

Язык: Английский

Процитировано

1

The combination of flaxseed lignans and PD-1/ PD-L1 inhibitor inhibits breast cancer growth via modulating gut microbiome and host immunity DOI Creative Commons

Hao Wu,

J.F. Liu, Xinghua Zhang

и другие.

Drug Resistance Updates, Год журнала: 2025, Номер 80, С. 101222 - 101222

Опубликована: Фев. 28, 2025

Patients with breast cancer (BC) who benefit from the PD-1/PD-L1 inhibitor (PDi) is limited, necessitating novel strategies to improve immunotherapy efficacy of BC. Here we aimed investigate inhibitory effects flaxseed lignans (FL) on biological behaviors BC and evaluate roles FL in enhancing anticancer PDi. HPLC was used detect content enterolactone (ENL), bacterial transformation product FL. Transcript sequencing performed identified CD38 as a downstream target gene ENL. CD38-overexpressing cells were constructed cell proliferation, colony formation, wound healing transwell assays assess function ENL/CD38 axis vitro. Multiplexed immunohistochemistry (mIHC) CyTOF changes tumor immune microenvironment (TIM). 16S rDNA explore gut microbiota mice. A series vivo experiments conducted mechanisms converted ENL by administration inhibited progression malignant downregulating CD38, key associated immunosuppression blockade resistance. The mIHC assay revealed that enhanced CD3+, CD4+ CD8+ reduced F4/80+ TIM. confirmed regulatory combination PDi (FLcPDi) In addition, analysis demonstrated FLcPDi treatment significantly elevated abundance Akkermansia and, importantly, response mice treated antibiotics. FL/ENL/CD38 progression. modulating host immunity.

Язык: Английский

Процитировано

1

The axis of tumor-associated macrophages, extracellular matrix proteins, and cancer-associated fibroblasts in oncogenesis DOI Creative Commons
Shu‐Hong Yu, Siyu Wang, Xuanyu Wang

и другие.

Cancer Cell International, Год журнала: 2024, Номер 24(1)

Опубликована: Окт. 7, 2024

The extracellular matrix (ECM) is a complex, dynamic network of multiple macromolecules that serve as crucial structural and physical scaffold for neighboring cells. In the tumor microenvironment (TME), ECM proteins play significant role in mediating cellular communication between cancer-associated fibroblasts (CAFs) tumor-associated macrophages (TAMs). Revealing modification TME necessitates intricate signaling cascades transpire among diverse cell populations proteins. advent single-cell sequencing has enabled identification refinement specific subpopulations, which substantially enhanced our comprehension milieu given us high-resolution perspective on diversity However, it essential to integrate data establish coherent framework. this regard, we present comprehensive review relationships ECM, TAMs, CAFs. This encompasses insights into released by TAMs CAFs, integration TAM-ECM-CAF axis, potential applications limitations targeted therapies serves reliable resource focused therapeutic strategies while highlighting intermediates TME.

Язык: Английский

Процитировано

7

LINC01089 in cancer: multifunctional roles and therapeutic implications DOI Creative Commons

Qiang Yi,

Gangfeng Zhu,

Xinting Ouyang

и другие.

Journal of Translational Medicine, Год журнала: 2024, Номер 22(1)

Опубликована: Сен. 27, 2024

Язык: Английский

Процитировано

5

Parishin B blocking TRIB3-AKT1 interaction inhibits breast cancer lung metastasis DOI Creative Commons

Xiongtao Cheng,

Jianguo Sun, Shouhong Chen

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 15

Опубликована: Янв. 15, 2025

TRIB3 has been reported to mediate breast cancer (BC) proliferation and metastasis by interacting with AKT1, blocking the interaction between AKT1 can inhibit progression of BC. Besides, inhibiting turn "cold tumor" hot also proved be an effective therapeutic strategy for Thus, this study aim find drugs that bind BC progression, further elucidate its mechanism. The possible inhibitors were screened high-throughput molecular docking, CETSA, CO-IP assay. Then, effect inhibitor anti was assessed CCK-8 assay, flow cytometry, plate colony formation transwell assay; RNA-seq empolyed potential mechanism Parishin B (PB) anti-BC. Finally, on lung in vivo evaluated. PB as a TRIB3, CETSA assay indicated could target block TRIB3-AKT1 interaction. In addition, exhibited good anti-BC activity without drug toxicity normal cells experiments vitro, analysis suggested invasion related cell cycle. It vivo. demonstrated regulating cycle, providing agent treatment

Язык: Английский

Процитировано

0

The construction of a breast cancer prognostic model by combining genes related to hypoxia and endoplasmic reticulum stress DOI
Guohua Liu, Yuan Shi, Jing Wang

и другие.

Computer Methods in Biomechanics & Biomedical Engineering, Год журнала: 2025, Номер unknown, С. 1 - 14

Опубликована: Янв. 27, 2025

Breast cancer (BC) is a malignant tumor that occurs in breast tissue. This project aims to predict the prognosis of BC patients using genes related hypoxia and endoplasmic reticulum stress (ERS). RNA-seq clinical data for were downloaded from TCGA GEO databases. Hypoxia ERS-related collected Genecards database. Univariate/multivariate Cox regression Lasso analyses used screen construct prognostic models. Patients divided into high-risk (HR) low-risk (LR) groups based on risk scores. The CIBERSORT algorithm was analyze differences immune infiltration between two groups. mutations analyzed statistically. CellMiner database drug prediction TISCH single-cell sequencing analysis. We screened 8 feature model. HR group had remarkably worse prognosis. TP53 exhibited higher mutation frequency group. analysis uncovered remarkable increase levels Macrophages M0 Tregs patients. Drug sensitivity demonstrated expression IVL greatly negatively linked with COLCHICINE. PTGS2 negative correlation Vincristine sensitivity. model can survival, status, potential drugs patients, bringing new perspective individualized treatment.

Язык: Английский

Процитировано

0