Fatty acid metabolism: A new target for nasopharyngeal carcinoma therapy DOI Open Access
Juan Li,

Pengbin Ping,

Yanhua Li

et al.

Chinese Journal of Cancer Research, Journal Year: 2024, Volume and Issue: 36(6), P. 652 - 668

Published: Jan. 1, 2024

Lipid metabolic reprogramming is considered one of the most prominent abnormalities in cancer, and fatty acid metabolism a key aspect lipid metabolism. Recent studies have shown that its related pathways play important roles malignant progression nasopharyngeal carcinoma (NPC). NPC cells adapt to harsh environments by enhancing biological processes such as metabolism, uptake, production, oxidation, thereby accelerating their growth. In addition, plays central role tumor microenvironment (TME) NPC, phenotypic transformation immune closely Moreover, contributes escape, which significantly affects disease treatment, progression, recurrence, metastasis. This review explores recent advances focuses on interconnections among reprogramming, immunity, corresponding therapies. conclusion, represents potential target for further exploration needed develop strategies interaction between immunotherapy.

Language: Английский

Protective effects and mechanisms of quercetin in animal models of hyperuricemia: A systematic review and meta-analysis DOI Creative Commons

Xueren Bian,

Z. K. Ge,

Xu-Shan Chen

et al.

Pharmacological Research, Journal Year: 2025, Volume and Issue: unknown, P. 107665 - 107665

Published: Feb. 1, 2025

Quercetin, a prevalent natural flavonoid found in various medicinal plants, including Dendrobium officinale Kimura & Migo, has garnered attention for its potential health benefits. However, foundational animal studies investigating the effects of quercetin on lowering uric acid levels remain insufficiently established, and number related clinical is limited. This scarcity hinders practical application managing hyperuricemia. We systematically searched preclinical published by December 2024 nine databases, such as PubMed, Web Science, Embase. The results our meta-analysis showed that, compared with model group, not only effectively alleviated pathological injury kidney liver improved renal function indexes hyperuricemia but also played role modulating multiple signaling pathways oxidative stress, lipid metabolism, transporter proteins. Quercetin more substantial effect decreasing serum creatinine (SMD = -4.29, 95% CI [-6.48, -2.10], P 0.0001), blood urea nitrogen -3.08, [-4.80, -1.35], 0.0005), Up-regulate organic anion 1 mRNA expression 2.72, 95%CI [0.45, 4.99], 0.02) to positive control group. Sensitivity analyses confirmed stability results, while subgroup analysis indicates that treatment course may be main source heterogeneity. Dose-efficacy suggested had protective against at gavage dose 100 - 200mg/kg. accurately assess hyperuricemia, it essential conduct additional high-quality, large-scale trials validate findings.

Language: Английский

Citations

1
Isocucurbitacin B Inhibits Gliomas Through the Promotion of Anoikis by Targeting Caveolin 1 DOI
Mingyu Han,

Pingting Chen,

Fu Peng

et al.

Published: Jan. 1, 2025

Gliomas are devastating, incurable malignant tumors with high recurrence rates and frequent treatment failures due to their resistance complete surgical resection. We found that isocucurbitacin B significantly inhibited the proliferation, invasion, migration, epithelial-mesenchymal transition (EMT) of glioma cells by downregulating expression MMP2, N-cadherin, vimentin. Moreover, reduced CDK1 cyclin A2, resulting in G2/M phase arrest U251 cells. Isocucurbitacin induced apoptosis increasing cleaved caspase-3 BAX/BCL-2 ratio levels. Simultaneously, promoted anoikis decreasing caveolin 1, focal adhesion kinase phosphorylation, tropomyosin receptor The cellular thermal shift assay further confirmed direct binding 1. Additionally, activated BKCa calcium channel cells, leading increased intracellular Ca2+ levels decreased pH. In vivo, tumor growth zebrafish patient-derived xenograft situ mouse models. Our results suggest a potential link between ion channels highlight role cholesterol metabolism regulation. promising B's as therapeutic agent gliomas.

Language: Английский

Citations

0
Metabolic reprogramming and signaling adaptations in anoikis resistance: mechanisms and therapeutic targets DOI
Chao He, Jie He

Molecular and Cellular Biochemistry, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 16, 2025

Language: Английский

Citations

0
Prunella vulgaris Polyphenols Alleviate Liver Injury-Uveitis Comorbidity by Regulating Acylcarnitine via the S100A9-PP2A-AMPK Pathway DOI
Jingchen Xie,

Suhui Xiong,

Jiahui Yu

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156675 - 156675

Published: March 1, 2025

Language: Английский

Citations

0
CAMKKβ supports growth and viability of epithelial ovarian cancer in vitro and in vivo DOI
Matthew J. Borrelli,

Adrian Buensuceso,

Yudith Ramos-Valdes

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: April 17, 2025

Abstract Epithelial ovarian cancer (EOC) metastasizes predominantly through multicellular aggregates known as spheroids, which disseminate within the peritoneal cavity and initiate secondary disease upon reattachment at distant sites. EOC spheroids resist detachment-induced cell death by upregulating stress responses including AMP-activated protein kinase (AMPK) signaling AMPK-dependent macroautophagy (autophagy), highlighting these pathways potential therapeutic targets. Previously, we used a pharmacological approach to putatively identify Ca2+/calmodulin-dependent 2 (CAMKKβ, encoded CAMKK2) primary activator of AMPK in spheroids. Herein have generated CAMKK2 knockout lines via CRISPR–Cas9 genome editing confirm this function CAMKKβ explore impacts its loss using vitro vivo models metastatic EOC. exhibited decreased activation, autophagic flux, viability, relative parental intraperitoneal xenograft tumours lacking grew slower than their CAMKKβ-intact counterparts. Effect magnitudes varied between line models, suggesting context-dependent roles for rationalizing further studies characterize underlying mechanisms. Altogether, our findings highlight an important contributor metabolic reprogramming target setting advanced disease.

Language: Английский

Citations

0
Identification of Anoikis‐Related Genes in Gastric Cancer: Bioinformatics and Experimental Validation DOI Creative Commons

Chao Song,

Wenbo Liu,

Xiaoyu Wang

et al.

Cancer Medicine, Journal Year: 2025, Volume and Issue: 14(8)

Published: April 1, 2025

ABSTRACT Introduction Distant metastasis is the main reason for poor prognosis of gastric cancer, and anoikis refers to cell death caused when cells detach from extracellular matrix or adhere in incorrect locations, playing an important role distant cancer. Methods Download TCGA‐STAD dataset gene set, filter out differentially expressed genes. Perform consensus clustering cancer samples, conduct Weighted Gene Correlation Network Analysis (WGCNA), enrichment analysis, immune infiltration analysis expression characteristics each subtype, while also filtering genes with differential between subtypes. Additionally, through COX survival identify related establish a nomogram. Finally, validate CYP1B1 vivo vitro clinical culture, establishment model. Results Three subtypes were identified, exhibiting different characteristics, biological pathways, infiltration. The abundance activated NK cells, memory B M2 macrophages showed significant differences among three We screened four sets five (CYP1B1, EQTN, NRXN2, TBC1D3E, TCEAL5) Through we identified 33 independent prognostic constructed nomogram, calibration curves indicating good consistency. selected experimental validation, experiments demonstrated that highly participates resistance promotes invasion, migration, tumor progression cells. Conclusion patterns based on vary, providing theoretical support future personalized treatment

Language: Английский

Citations

0
Anoikis Resistance in Cancer: Mechanisms, Therapeutic Strategies, Potential Targets, and Models for Enhanced Understanding DOI
Pallab Shaw, Arpan Dey Bhowmik, Mohan Shankar Gopinatha Pillai

et al.

Cancer Letters, Journal Year: 2025, Volume and Issue: unknown, P. 217750 - 217750

Published: April 1, 2025

Language: Английский

Citations

0
Inhibiting FAT1 Blocks Metabolic Bypass to Enhance Antitumor Efficacy of TCA Cycle Inhibition through Suppressing CPT1A‐Dependent Fatty Acid Oxidation DOI Creative Commons
Fanghui Chen, Jianqiang Yang,

David O. Popoola

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: May 23, 2025

Abstract FAT atypical cadherin 1 ( FAT1 ) is one of the most frequently mutated genes in head and neck squamous cell carcinoma (HNSCC), exhibiting highest mutation rate across different tumor types. Although FAT1's role has attracted considerable attention, its impact on cancer metabolism treatment resistance remains poorly understood. In this study, it demonstrated that knockout mutant HNSCC cells attenuates CPT1A‐driven fatty acid oxidation (FAO) through downregulation transcription factor ASCL2, leading to marked suppression growth. Notably, ‐mutant exhibit TCA cycle inhibitor CPI‐613 activation CPT1A‐mediated FAO, whereas genetic ablation restores sensitivity CPI‐613. To achieve vivo depletion , LNP‐sgFAT1 developed, a novel lipid nanoparticle (LNP) system encapsulating Cas9 mRNA ‐targeting sgRNA. murine models bearing tumors, enhanced antitumor activity when combined with Collectively, these findings establish drives CPT1A‐dependent facilitating metabolic bypass confers inhibition HNSCC. This mechanistic insight highlights promising opportunities for combinatorial therapeutic strategies co‐targeting vulnerabilities cancer.

Language: Английский

Citations

0
Fatty acid metabolism: A new target for nasopharyngeal carcinoma therapy DOI Open Access
Juan Li,

Pengbin Ping,

Yanhua Li

et al.

Chinese Journal of Cancer Research, Journal Year: 2024, Volume and Issue: 36(6), P. 652 - 668

Published: Jan. 1, 2024

Lipid metabolic reprogramming is considered one of the most prominent abnormalities in cancer, and fatty acid metabolism a key aspect lipid metabolism. Recent studies have shown that its related pathways play important roles malignant progression nasopharyngeal carcinoma (NPC). NPC cells adapt to harsh environments by enhancing biological processes such as metabolism, uptake, production, oxidation, thereby accelerating their growth. In addition, plays central role tumor microenvironment (TME) NPC, phenotypic transformation immune closely Moreover, contributes escape, which significantly affects disease treatment, progression, recurrence, metastasis. This review explores recent advances focuses on interconnections among reprogramming, immunity, corresponding therapies. conclusion, represents potential target for further exploration needed develop strategies interaction between immunotherapy.

Language: Английский

Citations

0