Single-Cell Transcriptome Analysis Reveals Paraspeckles Expression in Osteosarcoma Tissues DOI
Emel Rothzerg, Wenyu Feng, Dezhi Song

et al.

Cancer Informatics, Journal Year: 2022, Volume and Issue: 21

Published: Jan. 1, 2022

Nuclear paraspeckles are subnuclear bodies contracted by nuclear-enriched abundant transcript 1 (NEAT1) long non-coding RNA, localised in the interchromatin space of mammalian cell nuclei. Paraspeckles have been critically involved tumour progression, metastasis and chemoresistance. To this date, there limited findings to suggest that paraspeckles, NEAT1 heterogeneous nuclear ribonucleoproteins (hnRNPs) directly or indirectly play roles osteosarcoma progression. Herein, we analysed NEAT1, paraspeckle proteins (SFPQ, PSPC1 NONO) hnRNP members (HNRNPK, HNRNPM, HNRNPR HNRNPD) gene expression 6 tissues using single-cell RNA-sequencing method. The normalised data highlighted transcripts were highly osteoblastic OS cells, except which was expressed myeloid 2 subpopulations.

Language: Английский

lncRNA NEAT1: Key player in neurodegenerative diseases DOI Creative Commons
Kun Li, Ziqiang Wang

Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 86, P. 101878 - 101878

Published: Feb. 3, 2023

Neurodegenerative diseases are the most common causes of disability worldwide. Given their high prevalence, devastating symptoms, and lack definitive diagnostic tests, there is an urgent need to identify potential biomarkers new therapeutic targets. Long non-coding RNAs (lncRNAs) have recently emerged as powerful regulatory molecules in neurodegenerative diseases. Among them, lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported be upregulated Alzheimer's disease (AD), Parkinson's (PD), Huntington's (HD), amyotrophic lateral sclerosis (ALS). However, whether this part a protective or harmful mechanism still unclear. This review summarizes our current knowledge role NEAT1 its association with characteristic aggregation misfolded proteins: amyloid-β tau AD, α-synuclein PD, mutant huntingtin HD, TAR DNA-binding protein-43 fused sarcoma/translocated liposarcoma ALS. The aim stimulate further research on more precise effective treatments for

Language: Английский

Citations

68

Exploring the role of lncrna neat1 knockdown in regulating apoptosis across multiple cancer types: A review DOI
Md Sadique Hussain, Gaurav Gupta, Muhammad Afzal

et al.

Pathology - Research and Practice, Journal Year: 2023, Volume and Issue: 252, P. 154908 - 154908

Published: Oct. 31, 2023

Language: Английский

Citations

54

Unraveling NEAT1's complex role in lung cancer biology: a comprehensive review. DOI
Md Sadique Hussain, Obaid Afzal, Gaurav Gupta

et al.

PubMed, Journal Year: 2024, Volume and Issue: 23, P. 34 - 52

Published: Jan. 1, 2024

This review delves into the pivotal role of long non-coding RNA NEAT1 in cancer biology, particularly lung (LC). It emphasizes NEAT1's unique subcellular localization and active involvement gene regulation chromatin remodeling. The highlights impact on LC development progression, including cell processes such as proliferation, migration, invasion, resistance to therapy, positioning it a potential diagnostic marker therapeutic target. complex web regulatory interactions with proteins microRNAs is explored, alongside challenges targeting therapeutically. concludes optimistically, suggesting future avenues for research personalized therapies, shedding light crucial LC. See also Graphical abstract(Fig. 1).

Language: Английский

Citations

30

N6‐methyladenosine reader hnRNPA2B1 recognizes and stabilizes NEAT1 to confer chemoresistance in gastric cancer DOI Creative Commons
Jiayao Wang, Jiehao Zhang, Hao Liu

et al.

Cancer Communications, Journal Year: 2024, Volume and Issue: 44(4), P. 469 - 490

Published: March 21, 2024

Abstract Background Chemoresistance is a major cause of treatment failure in gastric cancer (GC). Heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) an N6‐methyladenosine (m 6 A)‐binding protein involved variety cancers. However, whether m A modification and hnRNPA2B1 play role GC chemoresistance largely unknown. In this study, we aimed to investigate the downstream mechanism chemoresistance. Methods The expression among public datasets were analyzed validated by quantitative PCR (qPCR), Western blotting, immunofluorescence, immunohistochemical staining. biological functions investigated both vitro vivo. RNA sequencing, methylated immunoprecipitation, stability assay performed assess association between binding RNA. maintenance stemness was evaluated bioinformatic analysis, qPCR, sphere formation assays. patterns regulators specimens from patients who received adjuvant chemotherapy RNAscope multiplex immunohistochemistry. Results Elevated found cells tissues, especially multidrug‐resistant (MDR) cell lines. associated with poor outcomes patients, those 5‐fluorouracil treatment. Silencing effectively sensitized inhibiting proliferation inducing apoptosis Mechanically, interacted stabilized long noncoding NEAT1 A‐dependent manner. Furthermore, worked together enhance properties via Wnt/β‐catenin signaling pathway. clinical subjected chemotherapy, levels hnRNPA2B1, NEAT1, CD133, CD44 markedly elevated non‐responders compared responders. Conclusion Our findings indicated that interacts stabilizes lncRNA which contribute property pathway exacerbate GC.

Language: Английский

Citations

16

LncRNA NEAT1 facilitates glioma progression via stabilizing PGK1 DOI Creative Commons
Jingshan Liang, Changtao Liu,

Dezhi Xu

et al.

Journal of Translational Medicine, Journal Year: 2022, Volume and Issue: 20(1)

Published: Feb. 5, 2022

Abstract Background Long noncoding RNA NEAT1 has been implicated in glioma progression. However, the effect of on glycolysis cell and potential mechanism remain unclear. Methods In vitro experiments, including CCK-8, colony formation, ECAR, lactate detection assays were performed to evaluate proliferation cell. pulldown RIP identify interaction between PGK1. Truncated mutation PGK1 was used confirm specific interactive domains Animal studies analyze NEAT1/PGK1 Results knockdown significantly suppressed cells. could specifically interact with PGK1, which promotes stability. Hairpin A is essential for M1 domain Depletion markedly inhibited tumor growth mice, while reverse this effect. Higher expression associated poor overall survival GBM patients. Conclusions over progression through stabilizing axis a candidate therapeutic target treatment.

Language: Английский

Citations

52

Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation DOI Creative Commons
Yongli Pan, Ting Wang, Zhiqiang Zhao

et al.

Journal of Inflammation Research, Journal Year: 2022, Volume and Issue: Volume 15, P. 557 - 571

Published: Jan. 1, 2022

Abstract: Nuclear paraspeckle assembly transcript 1 (Neat1) located at chromosome 11 is a long non-coding RNA that widely expressed in mammalian cell types, and which overexpressed several inflammation-related disorders. Inflammation implies plethora of mutual interactions between both soluble factors cells due to various stimuli including tissue injury. Although there no doubt inflammation critically involved multiple biological pathological processes alike, the precise mechanisms being are still open for debate. In this context, role Neat1 as regulator inflammation, microglial activation, lipid accumulation under inflammatory conditions remains elusive. Herein, we review regulation how it modulates expression its target genes. Thereafter, will impact on by activating or inhibiting signaling pathways, such microRNAs, AKT, TLR4, TRAF6, NF-κB. Keywords: Neat1, microglia, lipids, microRNA, NF-κB

Language: Английский

Citations

38

NEAT1_1 confers gefitinib resistance in lung adenocarcinoma through promoting AKR1C1-mediated ferroptosis defence DOI Creative Commons

Shuman Zhen,

Yunlong Jia, Yan Zhao

et al.

Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: March 12, 2024

Abstract Gefitinib is one of the most extensively utilized epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) for treating advanced lung adenocarcinoma (LUAD) patients harboring EGFR mutation. However, emergence drug resistance significantly compromised clinical efficacy EGFR-TKIs. Gaining further insights into molecular mechanisms underlying gefitinib holds promise developing novel strategies to overcome and improve prognosis in LUAD patients. Here, we identified that inhibitory on EGFR-mutated cells was partially dependent induction ferroptosis, ferroptosis protection resulted resistance. Among suppressors, aldo-keto reductase family 1 member C1 (AKR1C1) exhibited significant upregulation gefitinib-resistant strains predicted poor progression-free survival (PFS) overall (OS) who received first-generation EGFR-TKI treatment. Knockdown AKR1C1 reversed by re-sensitizing gefitinib-mediated ferroptosis. The decreased expression miR-338-3p contributed aberrant cells. Furthermore, upregulated long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1_1 (NEAT1_1) sponged neutralize its suppression AKR1C1. Dual-luciferase reporter assay miRNA rescue experiment confirmed NEAT1_1/miR-338-3p/AKR1C1 axis Gain- loss-of-function assays demonstrated promoted resistance, proliferation, migration, invasion This study reveals effects axis-mediated defence LUAD. Thus, targeting might be a strategy overcoming

Language: Английский

Citations

13

Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer DOI Open Access
Yun Ju Lee, Woo Ryung Kim, Eun Gyung Park

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(8), P. 4548 - 4548

Published: April 21, 2024

Colorectal cancer (CRC) is the third most prevalent to be diagnosed, and it has a substantial mortality rate. Despite numerous studies being conducted on CRC, remains significant health concern. The disease-free survival rates notably decrease as CRC progresses, emphasizing urgency for effective diagnostic therapeutic approaches. development caused by environmental factors, which mostly lead disruption of signaling pathways. Among these pathways, Wingless/Integrated (Wnt) pathway, Phosphatidylinositol 3-kinase/protein kinase B/mammalian target rapamycin (PI3K/AKT/mTOR) Mitogen-Activated Protein Kinase (MAPK) Transforming Growth Factor-β (TGF-β) p53 pathway are considered important. These pathways also regulated non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long (lncRNAs), circular (circRNAs). They have emerged crucial regulators gene expression in changing their levels. altered patterns ncRNAs been implicated progression development, suggesting potential targets. This review provides an overview five key regulation involved pathogenesis that studied identify promising avenues diagnosis treatment strategies.

Language: Английский

Citations

12

Puzzling out the role of MIAT LncRNA in hepatocellular carcinoma DOI Creative Commons

Rawan Amr Elmasri,

Alaa A. Rashwan,

Sarah Hany Gaber

et al.

Non-coding RNA Research, Journal Year: 2024, Volume and Issue: 9(2), P. 547 - 559

Published: Jan. 11, 2024

A non-negligible part of our DNA has been proven to be transcribed into non-protein coding RNA and its intricate involvement in several physiological processes highly evidenced. The significant biological role non-coding RNAs (ncRNAs), including long (lncRNAs) variously reported. In the current review, authors highlight multifaceted myocardial infarction-associated transcript (

Language: Английский

Citations

11

Exploring the therapeutic potential of quercetin in cancer treatment: Targeting long non-coding RNAs DOI
Farhad Sheikhnia, Ahmad Fazilat,

Vahid Rashidi

et al.

Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 260, P. 155374 - 155374

Published: May 29, 2024

Language: Английский

Citations

8