Subverting Attachment to Prevent Attacking: Alteration of Effector Immune Cell Migration and Adhesion as a Key Mechanism of Tumor Immune Evasion DOI Creative Commons
Marta Mastrogiovanni, Emmanuel Donnadieu, Rajiv Pathak

et al.

Biology, Journal Year: 2024, Volume and Issue: 13(11), P. 860 - 860

Published: Oct. 24, 2024

Cell adhesion regulates specific migratory patterns, location, communication with other cells, physical interactions the extracellular matrix, and establishment of effector programs. Proper immune control cancer strongly depends on all these events occurring in a highly accurate spatiotemporal sequence. In response to cancer-associated inflammatory signals, cells navigating bloodstream shift from their patrolling exploratory migration mode establish adhesive vascular endothelial cells. This interaction enables them extravasate through blood vessel walls access site. Further within tumor microenvironment (TME) are crucial for coordinating distribution situ mounting an effective anti-tumor response. this review, we examine how alterations cues context favor escape by affecting cell infiltration trafficking TME. We discuss mechanisms which tumors directly modulate patterns affect immunity evasion. also explore indirect that involve modifications TME characteristics, such as vascularization, immunogenicity, structural topography. Finally, highlight significance aspects designing more drug treatments cellular immunotherapies.

Language: Английский

Hyaluronic Acid-Based Drug Delivery Systems for Cancer Therapy DOI Creative Commons
Ekaterina Pashkina, М. В. Быкова,

M. T. Berishvili

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(2), P. 61 - 61

Published: Jan. 7, 2025

In recent years, hyaluronic acid (HA) has attracted increasing attention as a promising biomaterial for the development of drug delivery systems. Due to its unique properties, such high biocompatibility, low toxicity, and modifiability, HA is becoming basis creation targeted systems, especially in field oncology. Receptors overexpressed subpopulations cancer cells, one them, CD44, recognized molecular marker stem cells. This review examines role receptors health tumors analyzes existing HA-based systems their use various types cancer. The new will bring opportunities challenges anti-cancer therapy.

Language: Английский

Citations

2
New N-Alkylketonetetrahydroisoquinoline derivatives exhibits antitumor effect by HA-CD44 interaction inhibition in MDA-MB-231 breast cancer DOI

Meriem Chayah,

José M. Espejo-Román,

Laura Erviti-Marticorena

et al.

Bioorganic Chemistry, Journal Year: 2025, Volume and Issue: 156, P. 108212 - 108212

Published: Jan. 24, 2025

Language: Английский

Citations

0
Role of MLIP in burn-induced sepsis and insights into sepsis-associated cancer progression DOI Creative Commons
Zhiwei Li, Qian Wang, Ying Liu

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 14, 2025

Introduction Burn-induced sepsis is a critical clinical challenge marked by systemic inflammation, immune dysregulation, and high mortality. Macrophage-driven inflammatory pathways are central to pathogenesis, while cell metabolic reprogramming plays key role in both cancer progression. Methods Bioinformatics analyses using GEO, TCGA, GTEx datasets identified MLIP-modulated genes linked responses prognosis. In vitro , LPS-stimulated HUVEC cells were used study MLIP’s effects on inflammation macrophage function through viability, ROS levels, cytokine expression, qRT-PCR, immunofluorescence assays. Results associated with immune-related cancer. Epigenetic analysis showed MLIP expression regulated promoter methylation chromatin accessibility. Prognostic revealed impact survival outcomes across types. reduced oxidative stress, hyperactivation. Conclusions regulates immune-metabolic dynamics burn-induced sepsis, influencing activity stress. Its suggests as potential therapeutic target linking modulation Further research evasion tumor metabolism may inform novel strategies.

Language: Английский

Citations

0
CD44 variant exons induce chemoresistance by modulating cell death pathways DOI Creative Commons
M. R. Yanova, Е. В. Степанова, D. V. Maltseva

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: March 6, 2025

Cancer chemoresistance presents a challenge in oncology, often leading to treatment failure and disease progression. CD44, multifunctional cell surface glycoprotein, has garnered attention for its involvement various aspects of cancer biology. Through alternative splicing, CD44 can form isoforms with the inclusion only standard exons, typical normal tissue, or addition variant frequently expressed tissue associated chemoresistance. The functions involved regulation signaling pathways are being actively studied, significance specific exons modulating death pathways, central response cells chemotherapy, begins become apparent. This review provides comprehensive analysis association exons/total clinical outcomes patients undergoing chemotherapy. role v6, v9 others significant effect on patient chemotherapy by means key cellular such as apoptosis, ferroptosis autophagy modulation is further identified, their impact drug resistance highlighted. An overview trials aimed at targeting exon-containing provided, possible directions development CD44-targeted therapeutic strategies discussed.

Language: Английский

Citations

0
Identification of SURF4 and RALGAPA1 as promising therapeutic targets in glioblastoma and pan-cancer through integrative multi-omics, CRISPR-Cas9 screening and prognostic meta-analysis DOI Creative Commons
Fei Wang, Yuxuan Chen, Run Huang

et al.

Cancer Immunology Immunotherapy, Journal Year: 2025, Volume and Issue: 74(6)

Published: April 18, 2025

Glioblastoma (GBM) is the most aggressive and malignant type of primary brain tumor, with a median survival time less than two years uniformly poor prognosis, despite multimodal therapeutic approaches, which highlights an urgent need for novel targets. In this study, by integrative multi-omics analysis from CPTAC database, DepMap database seven independent GBM cohorts, four hub genes (CD44, SURF4, IGSF3 RALGAPA1) were identified as essential regulated cancer driver robust prognostic value. data public in-house cohorts validated that CD44 SURF4 might be synthetic lethal partners loss-of-function tumor suppressor genes. Analysis immune-related pathway activity revealed complex regulation relationships in microenvironment (TME). Further investigation on activity, immune therapy response drug sensitivity proposed emerged promising target GBM, even pan-cancer. Pan-cancer exploration suggested RALGAPA1 may gene. By screening first-generation second-generation (CCDC106, GAL3ST1, GDI2 HSF1) considered targets after mutation

Language: Английский

Citations

0
CD44 Variant Expression in Follicular Cell-Derived Thyroid Cancers: Implications for Overcoming Multidrug Resistance DOI Creative Commons
Benny Mosoane, Michelle McCabe, Brandon S. Jackson

et al.

Molecules, Journal Year: 2025, Volume and Issue: 30(9), P. 1899 - 1899

Published: April 24, 2025

Thyroid cancer (TC) is a significant global health issue that exhibits notable heterogeneity in incidence and outcomes. In low-resource settings such as Africa, delayed diagnosis limited healthcare access exacerbate mortality rates. Among follicular cell-derived thyroid cancers—including papillary (PTC), (FTC), anaplastic (ATC), poorly differentiated (PDTC) subtypes—the role of CD44 variants has emerged critical factor influencing tumor progression multidrug resistance (MDR). CD44, transmembrane glycoprotein, its splice (CD44v) mediate cell adhesion, migration, survival, contributing to stem (CSC) maintenance therapy resistance. Differential expression patterns isoforms across TC subtypes have shown diagnostic, prognostic, therapeutic implications. Specifically, CD44v6 PTC been correlated with metastasis aggressive behavior, while FTC, aids distinguishing malignant from benign lesions. Furthermore, contributes MDR through enhanced drug efflux via ABC transporters, apoptosis evasion, CSC the Wnt/β-catenin PI3K/Akt pathways. Targeted therapies against monoclonal antibodies, hyaluronic acid-based nanocarriers, gene-editing technologies hold promise overcoming MDR. However, despite mounting evidence supporting CD44-targeted strategies various cancers, research on this potential remains limited. This review synthesizes existing knowledge variant cancers highlights mitigate MDR, particularly high-burden regions, thereby improving patient outcomes survival.

Language: Английский

Citations

0
Hyaluronic Acid Conjugated Geraniol for Targeted Breast Cancer Therapy DOI Creative Commons

Han Yu,

Lingling Jiang,

Yindu Bai

et al.

Natural Product Communications, Journal Year: 2025, Volume and Issue: 20(5)

Published: May 1, 2025

Objectives: Geraniol, a natural compound found in various essential oils and plant extracts, has shown promising anti-cancer effects on multiple types of cancer. This study aimed to examine the properties hyaluronic acid (HA)-conjugated geraniol (HA-geraniol) specifically breast cancer cells. Methods: investigated HA-geraniol both murine 4T1 human MDA-MB-231 cell lines. Mitochondrial membrane potential loss, apoptosis-inducing ability, cycle arrest were evaluated using flow cytometry. Additionally, tandem mass tag (TMT)-based proteomics analysis was conducted identify differentially expressed proteins cells following treatment with HA-geraniol. An vivo efficacy carried out 4T1-bearing BALB/c mouse xenograft model assess therapeutic impact compared naked drug. Results: The vitro experiments demonstrated that exhibited superior It induce mitochondrial apoptosis, Proteomic revealed may mediate death by up-regulating ATF3 activating complement coagulation cascade pathways. Furthermore, indicated effectively suppressed tumor growth metastasis model, showcasing its as agent for therapy. Conclusion: findings from this suggest holds great promise an efficient therapy, demonstrating significant .

Language: Английский

Citations

0
Development of Dual-Targeted Mixed Micelles Loaded with Celastrol and Evaluation on Triple-Negative Breast Cancer Therapy DOI Creative Commons

Siying Huang,

Simeng Xiao,

Xuehao Li

et al.

Pharmaceutics, Journal Year: 2024, Volume and Issue: 16(9), P. 1174 - 1174

Published: Sept. 6, 2024

Considering that the precise delivery of Celastrol (Cst) into mitochondria to induce mitochondrial dysfunction may be a potential approach improve therapeutic outcomes Cst on TNBC, novel tumor dual-targeted mixed-micelle nano-system was fabricated via self-synthesized triphenylphosphonium-modified cholesterol (TPP-Chol) and hyaluronic acid (HA)-modified (HA-Chol). The Cst-loaded mixed micelles (Cst@HA/TPP-M) exhibited characteristics small particle size, negative surface potential, high drug loading up 22.8%, sustained release behavior. Compared assembled only by TPP-Chol (Cst@TPP-M), Cst@HA/TPP-M decreased hemolysis rate upgraded in vivo stability safety. In addition, series cell experiments using triple-negative breast cancer line MDA-MB-231 as model proved effectively increased cellular uptake through CD44-receptors-mediated endocytosis, amount three times free group. confocal results demonstrated successful endo-lysosomal escape effective transport triggered charge converse after HA degradation endo-lysosomes. group, significantly elevated ROS levels, reduced membrane promoted apoptosis, showing better induction effect dysfunction. imaging antitumor based MDA-MB-231-tumor-bearing nude mice showed facilitated enrichment at site, attenuated systemic distribution, polished efficacy compared with Cst. general, target system, co-constructed HA-Chol might provide promising strategy ameliorate TNBC.

Language: Английский

Citations

3
Platycodin D ameliorates polycystic ovary syndrome-induced ovarian damage by upregulating CD44 to attenuate ferroptosis DOI
Rui Ji,

Shujun Wang,

Xin Chen

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 224, P. 707 - 722

Published: Sept. 24, 2024

Language: Английский

Citations

2
Subverting Attachment to Prevent Attacking: Alteration of Effector Immune Cell Migration and Adhesion as a Key Mechanism of Tumor Immune Evasion DOI Creative Commons
Marta Mastrogiovanni, Emmanuel Donnadieu, Rajiv Pathak

et al.

Biology, Journal Year: 2024, Volume and Issue: 13(11), P. 860 - 860

Published: Oct. 24, 2024

Cell adhesion regulates specific migratory patterns, location, communication with other cells, physical interactions the extracellular matrix, and establishment of effector programs. Proper immune control cancer strongly depends on all these events occurring in a highly accurate spatiotemporal sequence. In response to cancer-associated inflammatory signals, cells navigating bloodstream shift from their patrolling exploratory migration mode establish adhesive vascular endothelial cells. This interaction enables them extravasate through blood vessel walls access site. Further within tumor microenvironment (TME) are crucial for coordinating distribution situ mounting an effective anti-tumor response. this review, we examine how alterations cues context favor escape by affecting cell infiltration trafficking TME. We discuss mechanisms which tumors directly modulate patterns affect immunity evasion. also explore indirect that involve modifications TME characteristics, such as vascularization, immunogenicity, structural topography. Finally, highlight significance aspects designing more drug treatments cellular immunotherapies.

Language: Английский

Citations

0