Metabolic reprogramming in cancer and senescence DOI Creative Commons
Yuzhu Zhang, J. Tang, Can Jiang

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(3)

Published: March 1, 2025

The rising trend in global cancer incidence has caused widespread concern, one of the main reasons being aging population. Statistical data show that and mortality rates a clear upward with age. Although there is commonality between dysregulated nutrient sensing, which features aging, metabolic reprogramming tumor cells, specific regulatory relationship not clear. This manuscript intends to comprehensively analyze senescence reprogramming; as well reveal impact key factors leading cellular on tumorigenesis. In addition, this review summarizes current intervention strategies targeting sensing pathways, clinical cases treating tumors characteristics existing nanodelivery research strategies. Finally, it also suggests sensible dietary habits for those who wish combat aging. conclusion, attempts sort out link metabolism provide new ideas treatment.

Language: Английский

Targeting Metabolic–Redox Nexus to Regulate Drug Resistance: From Mechanism to Tumor Therapy DOI Creative Commons
Yuke Wang,

Jingqiu He,

Shan Lian

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(7), P. 828 - 828

Published: July 10, 2024

Drug resistance is currently one of the biggest challenges in cancer treatment. With deepening understanding drug resistance, various mechanisms have been revealed, including metabolic reprogramming and alterations redox balance. Notably, mediates survival tumor cells harsh environments, thereby promoting development resistance. In addition, changes during pattern shift trigger reactive oxygen species (ROS) production, which turn regulates cellular metabolism, DNA repair, cell death, metabolism direct or indirect ways to influence sensitivity tumors therapies. Therefore, intersection ROS profoundly affects clarifying entangled may be beneficial for developing drugs treatment methods thwart this review, we will summarize regulatory mechanism on highlight recent therapeutic strategies targeting metabolic-redox circuits, dietary interventions, novel chemosynthetic drugs, combination regimens, delivery systems.

Language: Английский

Citations

4
Transketolase attenuates the chemotherapy sensitivity of glioma cells by modulating R-loop formation DOI Creative Commons
Minjie Fu, Mengli Zhang, Licheng Zhang

et al.

Cell Reports, Journal Year: 2025, Volume and Issue: 44(1), P. 115142 - 115142

Published: Jan. 1, 2025

Highlights•TKT attenuates the chemosensitivity in glioma independent of catalytic activity•Chemotherapeutic drugs promote TKT's nuclear translocation cells•TKT interacts with XRN2 to regulate resolution and removal R-loopsSummaryGlioblastoma (GBM) is a highly lethal malignant brain tumor poor survival rates, chemoresistance poses significant challenge treatment patients GBM. Here, we show that transketolase (TKT), metabolic enzyme pentose phosphate pathway (PPP), chemotherapy sensitivity cells manner activity. Mechanistically, chemotherapeutic can facilitate TKT protein from cytosol into nucleus, where physically R-loops. Depletion leads increased R-loop accumulation genome instability, increasing susceptibility chemotherapy. In conclusion, our study reveals non-metabolic function regulating dynamics, gliomas.Graphical abstract

Language: Английский

Citations

0
A Mitochondria‐Related Signature in Diffuse Large B‐Cell Lymphoma: Prognosis, Immune and Therapeutic Features DOI Creative Commons
Zhiwei Zhou, Jiabin Lu, Song‐Bin Guo

et al.

Cancer Medicine, Journal Year: 2025, Volume and Issue: 14(2)

Published: Jan. 1, 2025

ABSTRACT Background Distinctive heterogeneity characterizes diffuse large B‐cell lymphoma (DLBCL), one of the most frequent types non‐Hodgkin's lymphoma. Mitochondria have been demonstrated to be closely involved in tumorigenesis and progression, particularly DLBCL. Objective The purposes this study were identify prognostic mitochondria‐related genes (MRGs) DLBCL, develop a risk model based on MRGs machine learning algorithms. Methods Transcriptome profiles clinical information obtained from Gene Expression Omnibus (GEO) database. was defined using Least Absolute Shrinkage Selection Operator (Lasso) regression algorithm, its value further examined independent datasets. Patients stratified into two clusters scores, additionally nomogram generated score characteristics. pathway level, microenvironment, expression targeted therapy‐associated genes, response immunotherapy, drug sensitivity, somatic mutation status compared between clusters. Results Eighteen (DNM1L, PUSL1, CHCHD4, COX7A1, CPT1A, CYP27A1, POLDIP2, PCK2, MRPL2, PDK3, PDK4, MARC2, ACSM3, COA7, THNSL1, ATAD3B, C15orf48, TOMM70A) identified construct model. Remarkable discrepancies observed groups. high‐risk group had shorter overall survival, less immune infiltration, lower CD20 higher PD‐L1 than low‐risk group. Distinct responses immunotherapy predictive IC50 values found Conclusions We established novel signature by which also outstanding tumor microenvironment therapies.

Language: Английский

Citations

0
EMB-driven glioblastoma multiforme progression via the MCT4/GPX3 axis: therapeutic inhibition by Ganxintriol A DOI Creative Commons
Bo Cheng, Jing Liu, Ling Gao

et al.

Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)

Published: March 4, 2025

Embigin (EMB) is a transmembrane glycoprotein highly expressed in glioblastoma multiforme (GBM), yet its role GBM progression remains unclear. In this study, we investigate the function of intracellular EMB promoting and evaluate effect Ganxintriol A, traditional Chinese herbal extract, treatment. Bioinformatics datasets were utilized to assess expression prognostic value patients. vitro experiments such as PCR、western blot,CCK8,transwell,wound healing,clone formation flow cytometry assays conducted examine EMB's biological functions underlying mechanisms cell lines. Additionally, constructed subcutaneous tumor model nude mice evaluated medicine extract A on through vivo experiments. associated with poor prognosis overexpression accelerated progression, whereas knockdown had opposite effect. Further analysis revealed that upregulated epithelial-mesenchymal transition (EMT) glycolysis while maintaining glutathione (GSH) redox balance by inducing monocarboxylate transporter 4 (MCT4) peroxidase 3 (GPX3) expression. Treatment significantly downregulated expression, effectively inhibiting both vivo. This study highlights an independent biomarker for reveals novel mechanism which drives progression. identified promising therapeutic candidate

Language: Английский

Citations

0
Metabolic reprogramming in cancer and senescence DOI Creative Commons
Yuzhu Zhang, J. Tang, Can Jiang

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(3)

Published: March 1, 2025

The rising trend in global cancer incidence has caused widespread concern, one of the main reasons being aging population. Statistical data show that and mortality rates a clear upward with age. Although there is commonality between dysregulated nutrient sensing, which features aging, metabolic reprogramming tumor cells, specific regulatory relationship not clear. This manuscript intends to comprehensively analyze senescence reprogramming; as well reveal impact key factors leading cellular on tumorigenesis. In addition, this review summarizes current intervention strategies targeting sensing pathways, clinical cases treating tumors characteristics existing nanodelivery research strategies. Finally, it also suggests sensible dietary habits for those who wish combat aging. conclusion, attempts sort out link metabolism provide new ideas treatment.

Language: Английский

Citations

0