Emerging insights into the role of microRNAs regulation of ferroptosis in hepatocellular carcinoma DOI
Qi Zhang, Yingdan Zhang,

Shiyun Guo

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2024, Volume and Issue: 1871(3), P. 167642 - 167642

Published: Dec. 27, 2024

Language: Английский

Ferroptosis: a novel mechanism of cell death in ophthalmic conditions DOI Creative Commons
Yaqi Yang,

Yumeng Lin,

Zhongyu Han

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: June 27, 2024

Ferroptosis, a new type of programmed cell death proposed in recent years, is characterized mainly by reactive oxygen species and iron-mediated lipid peroxidation differs from death, such as apoptosis, necrosis, autophagy. Ferroptosis associated with variety physiological pathophysiological processes. Recent studies have shown that ferroptosis can aggravate or reduce the occurrence development diseases targeting metabolic pathways signaling tumors, ischemic organ damage, other degenerative related to peroxidation. Increasing evidence suggests closely linked onset progression various ophthalmic conditions, including corneal injury, glaucoma, age-related macular degeneration, diabetic retinopathy, retinal detachment, retinoblastoma. Our review current research on reveals significant advancements our understanding pathogenesis, aetiology, treatment these conditions.

Language: Английский

Citations

5

Targeting cell death mechanisms: the potential of autophagy and ferroptosis in hepatocellular carcinoma therapy DOI Creative Commons
Beibei Liu,

Ling Liu,

Yang Liu

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Sept. 9, 2024

Ferroptosis is a type of cell death that plays remarkable role in the growth and advancement malignancies including hepatocellular carcinoma (HCC). Non-coding RNAs (ncRNAs) have considerable impact on HCC by functioning as either oncogenes or suppressors. Recent research has demonstrated non-coding ability to control ferroptosis cells, hence impacting tumors resistance these cells drugs. Autophagy mechanism conserved throughout evolution maintaining balance body under normal settings. Nevertheless, occurrence dysregulation autophagy evident progression various human disorders, specifically cancer. dual roles cancer, potentially influencing both survival death. prevalent kind liver genetic mutations changes molecular pathways might worsen its advancement. The subject debate, it capacity repress promote tumor growth. activation can apoptosis, proliferation glucose metabolism, facilitate spread through EMT. Inhibiting hinder enhance respond treatment. regulated several signaling pathways, such STAT3, Wnt, miRNAs, lncRNAs, circRNAs. Utilizing anticancer drugs target may advantageous implications for efficacy cancer

Language: Английский

Citations

4

5-methylcytosine methylation of MALAT1 promotes resistance to sorafenib in hepatocellular carcinoma through ELAVL1/SLC7A11-mediated ferroptosis DOI Creative Commons
Chuan-Jian Shi,

Fengxiang Pang,

Yuhe Lei

et al.

Drug Resistance Updates, Journal Year: 2024, Volume and Issue: 78, P. 101181 - 101181

Published: Dec. 4, 2024

Emerging evidence demonstrates that long non-coding RNAs (lncRNAs) play a crucial role in sorafenib resistance hepatocellular carcinoma (HCC), and lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is dysregulated sorafenib-resistant HCC cells. However, the underlying regulatory mechanisms of MALAT1 cells remain unclear. In present study, we demonstrated 5-methylcytosine (m5C) methylation catalyzed by NSUN2 ALYREF contributed to RNA stability upregulation MALAT1. The NSUN2/ALYREF/MALAT1 signaling axis was activated cells, inhibited sorafenib-induced ferroptosis drive resistance. Mechanistically, maintained mRNA SLC7A11 directly binding ELAVL1 stimulating its cytoplasmic translocation. Furthermore, explored new synergetic strategy for treatment combining inhibitor MALAT1-IN1 with sorafenib. results significantly enhanced efficacy both vitro vivo. Collectively, our work brings insights into epigenetic offers an alternative therapeutic targeting patients.

Language: Английский

Citations

4

Ferroptosis-related signaling pathways in cancer drug resistance DOI Open Access
Yang Yang‐Hartwich,

Simin Yu,

Wanyao Liu

et al.

Cancer Drug Resistance, Journal Year: 2025, Volume and Issue: 8(1)

Published: Jan. 6, 2025

Ferroptosis is an iron-dependent form of programmed cell death induced by lipid peroxidation. This process regulated signaling pathways associated with redox balance, iron metabolism, and metabolism. Cancer cells' increased demand makes them especially susceptible to ferroptosis, significantly influencing cancer development, therapeutic response, metastasis. Recent findings indicate that cells can evade ferroptosis downregulating key related this process, contributing drug resistance. underscores the possibility modulating as approach counteract resistance enhance efficacy. review outlines involved in their interactions cancer-related pathways. We also highlight current understanding resistance, offering insights into how targeting provide novel approaches for drug-resistant cancers. Finally, we explore potential ferroptosis-inducing compounds examine challenges opportunities development evolving field.

Language: Английский

Citations

0

TFAP2A-regulated CRNDE enhances colon cancer progression and chemoresistance via RIPK3 interaction DOI Creative Commons
Xin Gao, Yanming Huang, Tai Wei

et al.

Functional & Integrative Genomics, Journal Year: 2025, Volume and Issue: 25(1)

Published: Feb. 15, 2025

Colon cancer (CC) is a common malignancy with rising incidence worldwide. Despite advances in treatment strategies, many patients still face poor prognosis due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as important regulators various biological processes and been implicated progression. Among them, colorectal neoplasia differentially expressed (CRNDE) has drawn attention for its potential roles different cancers. However, specific functions CC remain unclear. In this study, we identified CRNDE highly CC, contributing tumor progression Mechanically, regulated by transcription factor TFAP2A. Additionally, inhibits pyroptosis, form programmed cell death, promoting ubiquitin-mediated degradation RIPK3, thereby reducing sensitivity cells 5-fluorouracil (5-FU). Our findings suggest that TFAP2A/CRNDE/RIPK3 axis plays critical colon chemoresistance, highlighting therapeutic targets improving outcomes.

Language: Английский

Citations

0

Comprehensive pan-cancer analysis identifies PLAG1 as a key regulator of tumor immune microenvironment and prognostic biomarker DOI Creative Commons

Ruicheng Wu,

Dengxiong Li, Shuxia Zhang

et al.

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

Published: April 10, 2025

Background The literature on the role of pleomorphic adenoma gene 1 (PLAG1) in malignant tumors is limited. This study aimed to perform pan-cancer analysis PLAG1. Methods expression PLAG1 was analyzed by Human Protein Atlas (HPA). differential and prognosis were based TCGA data. relationship between tumor heterogeneity, stemness immune infiltration investigated. enrichment biological function bladder cancer analyzed. Results increased a variety significantly correlated with patients. Their levels associated key checkpoint genes (CD274, HAVCR2), stimulation factors (CD48, CD27). In cancer, functional indicated that involved epidermal related processes pathways. reduction can inhibit proliferation cells. Conclusions has potential be prognostic marker therapeutic target for patients tumors.

Language: Английский

Citations

0

MCM4 potentiates evasion of hepatocellular carcinoma from sorafenib-induced ferroptosis through Nrf2 signaling pathway DOI

Xujin Liu,

Fan Zhang, Yu‐Chen Fan

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 142, P. 113107 - 113107

Published: Sept. 13, 2024

Language: Английский

Citations

2

Mechanisms of sorafenib resistance in hepatocellular carcinoma DOI
Yuanjing Liang

Clinics and Research in Hepatology and Gastroenterology, Journal Year: 2024, Volume and Issue: 48(8), P. 102434 - 102434

Published: July 29, 2024

Language: Английский

Citations

1

Regulating ferroptosis by non-coding RNAs in hepatocellular carcinoma DOI Creative Commons

Lijie Sun,

Hongfei Cao,

Yanzhe Wang

et al.

Biology Direct, Journal Year: 2024, Volume and Issue: 19(1)

Published: Sept. 12, 2024

Ferroptosis, a unique type of regulated cell death plays vital role in inhibiting tumour malignancy and has presented new opportunities for treatment therapy hepatocellular carcinoma. Accumulating studies indicate that epigenetic modifications by non-coding RNAs, including microRNAs, long noncoding circular can determine cancer vulnerability to ferroptosis HCC. The present review first summarize the updated core molecular mechanisms ferroptosis. We then provide concised overview modification Finally, we recent progress understanding ncRNA-mediated on will promote our regulatory modulating HCC, highlighting novel strategies HCC through targeting ncRNA-ferroptosis axis.

Language: Английский

Citations

1

Protocatechuic acid relieves ferroptosis in hepatic lipotoxicity and steatosis via regulating NRF2 signaling pathway DOI Creative Commons

Yetong Feng,

Mengjiao Shi, Yi Zhang

et al.

Cell Biology and Toxicology, Journal Year: 2024, Volume and Issue: 40(1)

Published: Nov. 26, 2024

Ferroptosis represents a newly programmed cell death, and the process is usually accompanied with iron-dependent lipid peroxidation. Importantly, ferroptosis implicated in myriad of diseases. Recent literature suggests potential position pathogenesis metabolic dysfunction-associated fatty liver disease (MAFLD), most widespread ailment worldwide. Intriguingly, several functional genes pathways central to are regulated by nuclear factor erythroid-derived 2-like 2 (NRF2). In current work, we aim identify protocatechuic acid (PCA), primary metabolite antioxidant polyphenols, as potent NRF2 activator inhibitor hepatic lipotoxicity steatosis models. Herein, both NRF2+/+ NRF2−/− lines mice were used analyze importance PCA function, models induced palmitic high-fat diet respectively. Our results indicated that was mitigated intervention cells. Furthermore, exhibited therapeutic efficacy against ferroptosis, well steatosis. The protective role predominantly mediated through activation, potentially elucidating pivotal mechanism underlying PCA's impact on MAFLD. Additionally, augmented mitochondrial TCA cycle activity observed ameliorated PCA, part via NRF2-dependent pathways, further bolstering anti-ferroptosis properties. Collectively, our findings underscore alleviating inducing activation signaling pathway, offering promising strategy for therapy MAFLD related disorders.

Language: Английский

Citations

1