Lipid metabolism dysregulation for bone metastasis and its prevention DOI

Jyoti Poswal,

Chandi C. Mandal

Expert Review of Anticancer Therapy, Journal Year: 2025, Volume and Issue: unknown

Published: April 12, 2025

Bone metastasis often develops in advanced malignancies. Lipid metabolic dysregulation might play pivotal role cancer progression and subsequent deterioration of bone health at metastatic condition. In-depth understanding lipid reprogramming metastasized cells other stromal including marrow adipocyte (BMA) is an urgent need to develop effective therapy. This paper emphasizes providing overview multifaceted dysregulated lipids BMA association with by utilizing search terms metabolism, PubMed. study extends address mechanism linked metabolism various crucial genes (e.g. CSF-1, RANKL, NFkB NFATc1) involved metastasis. review examines therapeutic strategies targeting offer potential avenues disrupt lipid-driven On condition, molecules especially not only favors but also potentiate within cells. Distinct lipid-metabolism associated may act as biomarker, these challenging task for specific treatment. Curbing function resorption controlling drugs statins, omega-3 FA metformin) provide additional support curtail lipid-associated

Language: Английский

Aging and tumors: a dynamic interaction DOI Creative Commons
Yudi Zhang,

Siqiang Zhu,

Zhaodong Liu

et al.

Discover Oncology, Journal Year: 2025, Volume and Issue: 16(1)

Published: Jan. 21, 2025

Abstract Aging is an inevitable physiological process in organisms, and the development of tumors closely associated with cellular senescence. This article initially examines role senescence tumorigenesis, emphasizing correlation between telomere length—a marker senescence—and tumor risk. Concurrently, study explores expression levels senescence-associated markers, such as p16, p53, mTOR, context development. Additionally, investigates impact on organismal senescence, including effects immune system function metabolic processes. Ultimately, discussion potential application anti-aging strategies therapy considers possibility utilizing mechanisms a novel therapeutic approach for tumors. research provides insights into complex interplay development, suggesting future preventative measures interventions.

Language: Английский

Citations

0
Metabolic landscape and rewiring in normal hematopoiesis, leukemia and aging DOI
Hui Fang,

Eunsun Yu,

Chang Liu

et al.

Seminars in Cancer Biology, Journal Year: 2025, Volume and Issue: 111, P. 1 - 15

Published: Feb. 9, 2025

Language: Английский

Citations

0
Restoration of Transgelin 2 Expression Reverses Immune Escape in Ovarian Cancer: A Dawn for Immunotherapy DOI Creative Commons
Zhiqiang Wang, Ge Lou, Mingzhu Yin

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(4)

Published: March 30, 2025

In a seminal study published in Nature, Hwang et al. recently revealed for the first time that Transgelin 2 (TAGLN2) regulates lipid metabolism and antitumor function through interaction with fatty acid binding protein 5 (FABP5) CD8+ T cells [1]. The mechanism by which TAGLN2 is inhibited endoplasmic reticulum (ER) stress microenvironment of ovarian cancer (OC) leading to T-cell dysfunction was clarified, providing new target potential strategy improving immunotherapy solid tumors. Lipid plays an indispensable role activation, proliferation, execution effector functions [2]. As critical regulator metabolism, FABP5 efficiently coordinates uptake transport, sufficient energy substrates mitochondrial respiration cells, thereby ensuring their optimal bioenergetic status during immunity [3, 4]. However, significant gaps remain understanding regulatory mechanisms particularly within tumor-related contexts. Metastatic OC, refractory immunosuppressive tumor resistant multiple therapeutic approaches—including cell-based immunotherapies, exerts drives functional impairment tumor-infiltrating [5]. Consequently, elucidating molecular underlying immune evasion OC identifying targets capable reversing cell paramount enhancing efficacy patient prognosis. exact way (TME) inhibits unclear. demonstrated expression significantly downregulated both ascites tumors patients. addition, surface decreased from patients compared peripheral cancer-free individuals, although total intracellular levels were comparable. These results suggest may affect intratumoral repressing expression. Further experiments showed localization on activated cells. This allows take up extracellular acids fuel respiration, maintaining requirements emphasize central promoting FABP5-mediated uptake. What pathways link TME signals suppression?​ authors discovered ER response IRE1α-XBP1s signaling pathway. active form XBP1s can bind directly promoter region gene inhibit its transcription. Overexpression rescued deficits ER-stressed enhanced uptake, cytokines, promoted utilization under glucose-limited conditions (Figure 1). context such as chimeric antigen receptor (CAR) often demonstrate limited against malignancies. Could engineering overcome limitations current therapies?​ endocrine (CER) leverage two subunits follicle-stimulating hormone (FSH) specifically eliminate FSH-receptor positive (FSHR+) tumors, increased efficacy. exhibited persistence, expanded memory populations, superior control mouse models, independent PD-1 blockade. highlights metabolic checkpoint tunable node arm TME. study, time, unambiguously defines crucial metabolism. It discovers interacts maintain function, thus filling gap immunometabolism. research reveals stress-IRE1α-XBP1s pathway, escape. finding provides novel perspective escape mechanisms. Moreover, it improve immunotherapies CAR-T therapy, offering strategies effectiveness Of course, this has some limitations. researchers mainly relied model investigate related Although essential cannot be ignored differences physiology system between human body direct application clinical treatment. scope focused OC. given unique microenvironmental characteristics, pathogenesis, different patterns, roles, other differ. overexpressed have promising effects experiments, application's safety side still necessitate further evaluation. At same complex interactions yet explored depth, limit comprehensive optimization strategies. future, should more common characteristics microenvironments investigated depth clarify universality specificity. We comprehensively analyze network many pathways, costimulatory metabolic-related explore nodes. important factor consider development CAR therapy. To vigorously carry out trials TAGLN2-based combination therapy optimize parameters protocol. Explore biomarker develop personalized precise treatment we will mystery remodeling open paths developing All involved writing manuscript. Zhiqiang Wang Mingzhu Yin initiated conception outline. Ge Lou organized processed figure. read approved final thank BioRender (biorender.com) technical support drawing figures. work supported National Key R&D Programmes (NKPs) China (Grant No. 2022YFC3601800), Natural Science Foundation (nos. 82173238), Harbin Medical University Cancer Hospital (CN) Nn10 Project (Nn10py2017-01). nothing report. declare no conflicts interest.

Language: Английский

Citations

0
The rising influence of lipid metabolism in lung cancer: a global research perspective DOI Creative Commons
Chaoqun Wang, Ming Lei, Wei Wang

et al.

Frontiers in Oncology, Journal Year: 2025, Volume and Issue: 15

Published: March 31, 2025

Lung cancer is a prevalent malignant neoplasm globally and the leading cause of cancer-related mortality, posing significant threat to human health imposing considerable societal burden. Researchers have recently focused more on lipid metabolism in lung cancer. However, date, there has been no bibliometric analysis relation metabolism. This study used methods analyze link between Publications from 1995 2024 were sourced Web Science Core Collection (WoSCC). The Microsoft Excel, R-bibliometrix, CiteSpace, VOSviewer software visualize data. In this study, total 535 publications identified, with marked increase number observed post-2016. Both China United States exerted substantial influence domain. Notably, Chinese Academy Sciences Huazhong University Technology demonstrated leadership various aspects research related Professor Ana Ramirez de Molina Frontiers Oncology most productive authors journals respectively. Besides, keywords like "lipid metabolism", "lung cancer", "expression", "metabolism" "growth" central current are expected continue driving future trends studies. Research relationship was still its early stages. Targeting represented promising therapeutic strategy, as inhibiting key enzymes involved biosynthesis uptake potential impede progression mitigate drug resistance. first thoroughly summarize developments area over past thirty years, providing scholars updated insights identifying directions.

Language: Английский

Citations

0
Lipid metabolism dysregulation for bone metastasis and its prevention DOI

Jyoti Poswal,

Chandi C. Mandal

Expert Review of Anticancer Therapy, Journal Year: 2025, Volume and Issue: unknown

Published: April 12, 2025

Bone metastasis often develops in advanced malignancies. Lipid metabolic dysregulation might play pivotal role cancer progression and subsequent deterioration of bone health at metastatic condition. In-depth understanding lipid reprogramming metastasized cells other stromal including marrow adipocyte (BMA) is an urgent need to develop effective therapy. This paper emphasizes providing overview multifaceted dysregulated lipids BMA association with by utilizing search terms metabolism, PubMed. study extends address mechanism linked metabolism various crucial genes (e.g. CSF-1, RANKL, NFkB NFATc1) involved metastasis. review examines therapeutic strategies targeting offer potential avenues disrupt lipid-driven On condition, molecules especially not only favors but also potentiate within cells. Distinct lipid-metabolism associated may act as biomarker, these challenging task for specific treatment. Curbing function resorption controlling drugs statins, omega-3 FA metformin) provide additional support curtail lipid-associated

Language: Английский

Citations

0