MLLT3 Regulates Melanoma Stemness and Progression by Inhibiting HMGB1 Nuclear Entry and MAGEA1 M5C Modification DOI Creative Commons
Yaling Li, Hong Liu, Jingyi Li

и другие.

Advanced Science, Год журнала: 2024, Номер unknown

Опубликована: Дек. 24, 2024

Abstract Melanoma stem cells are a kind of with self‐renewal and multi‐directional differentiation potential. They one the key factors in occurrence, development metastasis melanoma. This study demonstrates that MLLT3 is transcription factor regulates stemness progression interacted HMGB1 to inhibit its entry into nucleus, YBX1 reading m 5 C MAGEA1 , thereby inhibiting mRNA stability directly transcribed P53 stemness, proliferation melanoma cells. further explored potential mechanism interaction between miR‐542‐3p/miR‐3922‐3p . Furthermore, scRNA‐seq knock‐out resulted important changes cell subsets, activating TP53 MAPK pathways transforming The results indicate suppressor gene melanoma, expected become target for therapy.

Язык: Английский

Writers, readers, and erasers RNA modifications and drug resistance in cancer DOI Creative Commons
Di Chen, Xinyu Gu,

Yeltai Nurzat

и другие.

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Авг. 30, 2024

Drug resistance in cancer cells significantly diminishes treatment efficacy, leading to recurrence and metastasis. A critical factor contributing this is the epigenetic alteration of gene expression via RNA modifications, such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), 5-methylcytosine (m5C), 7-methylguanosine (m7G), pseudouridine (Ψ), adenosine-to-inosine (A-to-I) editing. These modifications are pivotal regulating splicing, translation, transport, degradation, stability. Governed by "writers," "readers," "erasers," impact numerous biological processes progression, including cell proliferation, stemness, autophagy, invasion, apoptosis. Aberrant can lead drug adverse outcomes various cancers. Thus, targeting modification regulators offers a promising strategy for overcoming enhancing efficacy. This review consolidates recent research on role prevalent resistance, with focus m6A, m1A, m5C, m7G, Ψ, A-to-I Additionally, it examines regulatory mechanisms linked underscores existing limitations field.

Язык: Английский

Процитировано

16
o8G-modified circKIAA1797 promotes lung cancer development by inhibiting cuproptosis DOI Creative Commons
Haotian Xu,

Qingyun Zhao,

Dunyu Cai

и другие.

Journal of Experimental & Clinical Cancer Research, Год журнала: 2025, Номер 44(1)

Опубликована: Апрель 2, 2025

Abstract Background Lung cancer is a serious threat to human life and health, but effective screening treatment methods are lacking. Circular RNAs (circRNAs) have important biological functions closely related tumour development. Some studies shown that the 8-oxo-7,8-dihydroguanosine (o8G) modification plays key role in disease process, effect of o8G on circRNAs has not been elucidated. Moreover, cuproptosis novel mode cell death which copper ions directly promote protein aggregation disruption cellular metabolic pathways. The present study revealed circKIAA1797 occurs promotes lung development by inhibiting cuproptosis, provides new perspectives for epitranscriptomic therapeutic approaches cancer. Methods circRNA differential expression profiles were via RNA high-throughput sequencing, lines tissues was detected using qPCR. Experiments such as immunoprecipitation (o8G RIP) crosslinking (CLIP) performed explore presence circKIAA1797. regulation reader Y-box binding 1 (YBX1) explored nuclear–cytoplasmic fractionation, actinomycin D (Act D) stability experiments other experiments. silencing overexpression systems constructed vivo vitro Tagged affinity purification (TRAP), (RIP), coimmunoprecipitation (Co-IP), immunofluorescence (IF) staining subsequently conducted reveal molecular mechanism regulates Results This first YBX1 recognises ROS-induced modifications increases cytoplasmic circKIAA1797, associated with stage prognosis, significantly function both vitro. inhibits intracellular ferredoxin (FDX1) mRNA, decreasing FDX1 mRNA stability, expression, signal transducer activator transcription (STAT1) lipoyltransferase (LIPT1) transcription; moreover, closure mitochondrial permeability transition pore (mPTP), ultimately Conclusions an can inhibit proteins promoting mPTP closure, only theoretical basis in-depth understanding mechanisms also potential target treatment.

Язык: Английский

Процитировано

0
INTERPLAY BETWEEN EPIGENETICS, SENESCENCE AND CELLULAR REDOX METABOLISM IN CANCER AND ITS THERAPEUTIC IMPLICATIONS DOI Creative Commons

Geoffrey Balamurli,

Angeline Qiu Xia Liew,

Wee‐Wei Tee

и другие.

Redox Biology, Год журнала: 2024, Номер 78, С. 103441 - 103441

Опубликована: Ноя. 23, 2024

There is accumulating evidence indicating a close crosstalk between key molecular events regulating cell growth and proliferation, which could profoundly impact carcinogenesis its progression. Here we focus on reviewing observations highlighting the interplay epigenetic modifications, irreversible cycle arrest or senescence, cellular redox metabolism. Epigenetic alterations, such as DNA methylation histone dynamically influence tumour transcriptome, thereby impacting phenotype, survival, spread. Interestingly, acquisition of senescent phenotype can be triggered by changes, acting double-edged sword via ability to suppress tumorigenesis facilitating an inflammatory milieu conducive for cancer Concurrently, aberrant metabolism, function balance reactive oxygen species (ROS) generation intracellular anti-oxidant defences, influences signalling cascades genomic stability in cells serving critical link epigenetics senescence. Recognizing this intricate interconnection offers nuanced perspective therapeutic intervention simultaneously targeting specific modulating senescence dynamics, restoring homeostasis.

Язык: Английский

Процитировано

2
m5C RNA methylation: a potential mechanism for infectious Alzheimer’s disease DOI Creative Commons

Sisi Teng,

Cunqiao Han,

Jian Zhou

и другие.

Frontiers in Cell and Developmental Biology, Год журнала: 2024, Номер 12

Опубликована: Авг. 8, 2024

Alzheimer’s disease (AD) is a neurodegenerative disorder caused by variety of factors, including age, genetic susceptibility, cardiovascular disease, traumatic brain injury, and environmental factors. The pathogenesis AD largely associated with the overproduction accumulation amyloid-β peptides hyperphosphorylation tau protein in brain. Recent studies have identified presence diverse pathogens, viruses, bacteria, parasites, tissues patients, underscoring critical role central nervous system infections inducing pathological changes AD. Nevertheless, it remains unestablished about specific mechanism which lead to occurrence As an important post-transcriptional RNA modification, 5-methylcytosine (m 5 C) methylation regulates wide range biological processes, splicing, nuclear export, stability, translation, therefore affecting cellular function. Moreover, has been recently demonstrated that multiple pathogenic microbial are m C host. However, infectious still uncertain. Therefore, this review discusses mechanisms pathogen-induced summarizes research on molecular AD, thereby providing new insight into exploring underlying

Язык: Английский

Процитировано

1
NSUN2 methylates IRF4 to affect the capacity of macrophages attached to titanium implant on osteogenic differentiation of PDLSCs and angiogenesis of HUVECs in vitro DOI Creative Commons
Li Xiao, Dongxue Wu, Tingting Zhang

и другие.

BMC Oral Health, Год журнала: 2024, Номер 24(1)

Опубликована: Ноя. 13, 2024

We aimed to investigate the effect and underlying mechanism of titanium (Ti) implant on polarization macrophages subsequent effects osteogenic differentiation periodontal ligament stem cells (PDLSCs) angiogenesis human umbilical vein endothelial (HUVECs) affected by macrophages. Firstly, regulatory Ti macrophage was investigated. Levels M1 markers M2 in were evaluated immunofluorescence staining method qPCR analysis. The capacity PDLSCs cultured with supernatants each group Alizarin Red S (ARS) qPCR. Angiogenesis related genes also HUVECs To explore whether RNA m5C modification can modulate regulation angiogenesis, we analyzed main using dot blotting methods. interaction between NSUN2 IRF4 verified m5C-RIP, RIP, double-luciferase gene report experiments. Macrophages activated as under interference LPS, attached implants more easily action LPS. enhanced HUVECs. level up-regulated treated LPS down-regulated implant. Over-expression attenuated promotion Up-regulation weakened KEGG analysis suggested that enriched several inflammatory signaling pathways. Moreover, methylates affect Taken together, type be stimulated vitro, promoting through NSUN2-mediated methylation IRF4.

Язык: Английский

Процитировано

0
MLLT3 Regulates Melanoma Stemness and Progression by Inhibiting HMGB1 Nuclear Entry and MAGEA1 M5C Modification DOI Creative Commons
Yaling Li, Hong Liu, Jingyi Li

и другие.

Advanced Science, Год журнала: 2024, Номер unknown

Опубликована: Дек. 24, 2024

Abstract Melanoma stem cells are a kind of with self‐renewal and multi‐directional differentiation potential. They one the key factors in occurrence, development metastasis melanoma. This study demonstrates that MLLT3 is transcription factor regulates stemness progression interacted HMGB1 to inhibit its entry into nucleus, YBX1 reading m 5 C MAGEA1 , thereby inhibiting mRNA stability directly transcribed P53 stemness, proliferation melanoma cells. further explored potential mechanism interaction between miR‐542‐3p/miR‐3922‐3p . Furthermore, scRNA‐seq knock‐out resulted important changes cell subsets, activating TP53 MAPK pathways transforming The results indicate suppressor gene melanoma, expected become target for therapy.

Язык: Английский

Процитировано

0