Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 744, P. 151196 - 151196
Published: Dec. 17, 2024
Language: Английский
Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 744, P. 151196 - 151196
Published: Dec. 17, 2024
Language: Английский
Molecular Cancer, Journal Year: 2024, Volume and Issue: 23(1)
Published: Sept. 30, 2024
Language: Английский
Citations
18Molecular Cancer, Journal Year: 2025, Volume and Issue: 24(1)
Published: Feb. 25, 2025
Over the past decade, circular RNAs (circRNAs) have gained recognition as a novel class of genetic molecules, many which are implicated in cancer pathogenesis via different mechanisms, including drug resistance, immune escape, and radio-resistance. ExosomalcircRNAs, particular, facilitatecommunication between tumour cells micro-environmental cells, fibroblasts, other components. Notably, can reportedly influence progression treatment resistance by releasing exosomalcircRNAs. circRNAs often exhibit tissue- cancer-specific expression patterns, growing evidence highlights their potential clinical relevance utility. These molecules show strong promise biomarkers therapeutic targets for diagnosis treatment. Therefore, this review aimed to briefly discuss latest findings on roles mechanisms key various malignancies, lung, breast, liver, colorectal, gastric cancers, well haematological malignancies neuroblastoma.This will contribute identification new circRNA early cancer.
Language: Английский
Citations
2Circulation Research, Journal Year: 2025, Volume and Issue: unknown
Published: April 17, 2025
BACKGROUND: Circular RNAs (circRNAs) have been gradually revealed to regulate the progression of heart disease in depth, showing their clinical significance. However, a mass cardiac circRNAs still has not functionally characterized. We aimed explore potential candidates that are involved pathological hypertrophy. METHODS: Public substantial RNA-sequencing data were utilized search hypertrophy–related circRNAs. Cardiomyocyte hypertrophy vitro was induced by Ang II (angiotensin II) treatment. Mice subjected infusion induce vivo. Gain-of-function and loss-of-function assays conducted detect effect or proteins RESULTS: A circRNA derived from cdyl (chromodomain Y-like) gene screened out named circCDYL. Our results showed expression circCDYL primary rat cardiomyocytes significantly II. demonstrated effectively promoted cardiomyocyte vitro. CircCDYL could encode ≈100-aa truncated CDYL peptide (tCDYL-100), whose sequence highly overlaps full-length CDYL. The translation tCDYL-100 activated N6-methylation under prohypertrophic stimulation. fulfilled Mechanistically, competed with for binding REST (RE1-silencing transcription factor) further disrupted formation REST-CDYL-EHMT2 (euchromatic histone-lysine N-methyltransferase 2) transcriptional repression complex, resulting activation rhoa nppb . Silence mouse hearts inhibit II–induced hypertrophy, while forced cause CONCLUSIONS: In summary, our study uncovered an important circRNA-derived regulatory mechanism on mediated N6-methyladenosine-circRNA-histone methylation
Language: Английский
Citations
1Redox Biology, Journal Year: 2024, Volume and Issue: 75, P. 103270 - 103270
Published: July 18, 2024
Ferroptosis, driven by iron-dependent phospholipid peroxidation, is emerging as an intrinsic cancer defense mechanism. However, the regulatory networks involved in ferroptosis remain largely unknown. Here, we found that serine beta-lactamase-like protein (LACTB) inhibits liver progression regulating ferroptosis. LACTB downregulated cancer, and ectopic expression of markedly cell viability, colony formation, tumour growth. knockout exerts opposite effects. Further investigation revealed blocks HSPA8 transcription a p53-dependent manner, resulting elevation NCOA4-mediated ferritinophagy inhibition SLC7A11/GSH/GPX4 signalling, thereby triggering suppressing progression. Liver cells with endogenous mutation p53 binding site promoter exhibited increased resistance to inducers, ferroptosis-promoting effect was significantly weakened these mutant cells. Importantly, identified downstream target lenvatinib, adeno-associated virus-mediated overexpression knockdown notably enhance attenuate anti-tumour efficacy lenvatinib vivo, respectively. Taken together, our study reveals novel action provides potential therapeutic strategies for enhancing cancer.
Language: Английский
Citations
7Pharmacology & Therapeutics, Journal Year: 2024, Volume and Issue: 261, P. 108697 - 108697
Published: July 23, 2024
Language: Английский
Citations
5Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 31, 2025
Inflammatory bowel disease (IBD) is associated with oxidative stress and redox signaling disruption. It recently reported that proautophagic autophagy/beclin-1 regulator 1 (AMBRA1) a positive modulator of the NF-κB pathway promotes intestinal inflammation. However, its effect on state whether AMBRA1 regulated by remain unknown. In this study, it found functions as pro-oxidative factor increases in epithelial cells (IECs) vitro vivo. Mechanistically, N-terminal F1 domain required for to competitively interact NRF2, thereby antagonizing interaction between deubiquitinating protein 3 (DUB3) suppressing DUB3-mediated NRF2 deubiquitination, leading degradation. response H2O2 stimulation, ubiquitin-specific protease 7 (USP7) enhanced, facilitating USP7 deubiquitinate at K83 K86 stabilize AMBRA1. Notably, inhibitor, P5091, inhibits colitis Elevated expression inflamed colon tissues from ulcerative patients negatively correlated decreased levels. Overall, study identifies IECs provides redox-modulating therapeutic strategy targeting USP7/AMBRA1 IBD.
Language: Английский
Citations
0Biochemical Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 116875 - 116875
Published: March 1, 2025
Language: Английский
Citations
0Life Sciences, Journal Year: 2025, Volume and Issue: unknown, P. 123643 - 123643
Published: April 1, 2025
Language: Английский
Citations
0IntechOpen eBooks, Journal Year: 2025, Volume and Issue: unknown
Published: April 16, 2025
Human epidermal growth factor receptor 2 (HER2) is a transmembrane tyrosine kinase that plays pivotal role in the development and progression of cancers, particularly breast gastric cancers. While HER2 overexpression commonly attributed to gene amplification, recent studies indicate epigenetic modifications, such as DNA methylation, histone modification, non-coding RNA interference, are also critical regulating expression activity. This article will focus on relationship between modification.
Language: Английский
Citations
0Cellular & Molecular Biology Letters, Journal Year: 2024, Volume and Issue: 29(1)
Published: Nov. 16, 2024
RNA splicing is a fundamental step of gene expression. While constitutive removes introns and joins exons unbiasedly, alternative (AS) selectively determines the assembly to generate variants corresponding same transcript. The biogenesis circular RNAs (circRNAs) inextricably associated with AS. Back-splicing, biogenic process circRNA, special form In cancer, both AS circRNA deviate from original track. present review, we delve into intricate interplay between circRNAs in context cancer. relationship intricate, where modulates return regulate events. Beyond that, epigenetic posttranscriptional modifications concurrently circRNAs. On basis this modality, summarize current knowledge on how factors other binding proteins biogenesis, interact influence Specifically, feedback loop regulation events contributes greatly oncogenesis cancer progression. summary, resolving crosstalk will not only provide better insight biology but also provoke novel strategies combat
Language: Английский
Citations
3