METTL3‐mediated the m6A modification of SF3B4 facilitates the development of non‐small cell lung cancer by enhancing LSM4 expression DOI Creative Commons

Guangsi He,

Kangsheng Gu, Jie Wei

et al.

Thoracic Cancer, Journal Year: 2024, Volume and Issue: 15(11), P. 919 - 928

Published: March 10, 2024

Abstract Background Splicing factor B subunit 4 (SF3B4) has been confirmed to participate in the progression of many cancers and is considered be a potential target for non‐small cell lung cancer (NSCLC). Thus, role molecular mechanism SF3B4 NSCLC deserves further study. Methods Quantitative real‐time PCR western blot were employed detect mRNA protein levels SF3B4, Sm‐like (LSM4) methyltransferase‐like 3 (METTL3). Cell proliferation, apoptosis, invasion, migration stemness tested by counting kit‐8, colony formation, flow cytometry, transwell, wound healing, sphere formation assays. The interaction between METTL3 or LSM4 was MeRIP, RIP Co‐IP Mice xenograft models constructed assess effects on tumorigenesis. Results had high expression tissues associated with shorter overall survival patients. Knockdown suppressed stemness, while inducing apoptosis. promoted stability m6A modification, its knockdown inhibited growth, metastasis downregulating SF3B4. could interact LSM4, sh‐SF3B4‐mediated inhibition functions reversed overexpression. In addition, reduced restrained tumor this effect Conclusion METTL3‐stablized via positively regulating LSM4.

Language: Английский

FDX1 downregulation activates mitophagy and the PI3K/AKT signaling pathway to promote hepatocellular carcinoma progression by inducing ROS production DOI Creative Commons
Bo Sun, Peng Ding, Yinghui Song

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 75, P. 103302 - 103302

Published: Aug. 6, 2024

Mitochondrial dysfunction and metabolic reprogramming can lead to the development progression of hepatocellular carcinoma (HCC). Ferredoxin 1 (FDX1) is a small mitochondrial protein recent studies have shown that FDX1 plays an important role in tumor cuproptosis, but its HCC still elusive. In this study, we aim investigate expression novel functions HCC.

Language: Английский

Citations

17
m6A modified pre-miR-503-5P contributes to myogenic differentiation through the activation of mTOR pathway DOI

Yalong Su,

Kaiping Deng, Zhipeng Liu

et al.

International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: 294, P. 139517 - 139517

Published: Jan. 5, 2025

Language: Английский

Citations

1
Epigenetic modifications in early stage lung cancer: pathogenesis, biomarkers, and early diagnosis DOI Creative Commons

Lingfeng Bi,

Xin Wang, Jiayi Li

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(3)

Published: Feb. 21, 2025

Abstract The integration of liquid biopsy with epigenetic markers offers significant potential for early lung cancer detection and personalized treatment. Epigenetic alterations, including DNA methylation, histone modifications, noncoding RNA changes, often precede genetic mutations are critical in progression. In this study, we explore how biopsy, combined markers, can provide cancer, potentially predicting onset up to 4 years before clinical diagnosis. We discuss the challenges targeting regulators, which could disrupt cellular balance if overexploited, need maintaining key gene expressions therapeutic applications. This review highlights promise using early‐stage diagnosis, a focus on optimizing treatment strategies precision medicine.

Language: Английский

Citations

1
Association between methyltransferase-like 3 and non-small cell lung cancer: pathogenesis, therapeutic resistance, and clinical applications DOI Open Access
Xiaojuan Su,

Yi Feng,

Yi Qu

et al.

Translational Lung Cancer Research, Journal Year: 2024, Volume and Issue: 13(5), P. 1121 - 1136

Published: May 1, 2024

Abstract: Non-small cell lung cancer (NSCLC) is a malignant that with high incidence, recurrence, and mortality rates in human beings, posing significant threats to health. Moreover, effective early diagnosis of NSCLC remains limited primarily by the lack accurate biomarkers. Therefore, there an urgent need understand mechanisms underlying pathogenesis treatment failure. Methyltransferase-like 3 (METTL3) prototypical member family which its members transfer methyl groups. It has been implicated modulating NSCLC, as well conferring resistance therapeutics. The targeting METTL3 for reported. However, relationship between be demonstrated. In this review, we discuss relevant interrelationships summarising studies on pathogenesis, therapeutic resistance, clinical applications. Current research suggests upregulation expression propels tumorigenesis, progression, NSCLC. propose excellent candidate biomarker prognosis. Therapeutic potential treatment. This review provides summary association would valuable reference both basic research.

Language: Английский

Citations

7
Copper homeostasis and pregnancy complications: a comprehensive review DOI

Tong-Yu Peng,

Chenglin Liu, Yufeng Qian

et al.

Journal of Assisted Reproduction and Genetics, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 10, 2025

Language: Английский

Citations

0
Assessing the prognostic and therapeutic value of cuproptosis-related genes in colon adenocarcinoma patients DOI Creative Commons

Zhanhui Ye,

Yixian Song,

Mengqing Zhu

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: April 10, 2025

Colon adenocarcinoma (COAD) remains a major global health challenge with poor prognosis despite advances in treatment, underscoring the need for new biomarkers. As novel mode of cell death, cuproptosis is thought to be potentially involved development cancer. However, particularly as role cuproptosis-related genes (CRGs) COAD and therapy unclear. We analyzed RNA sequencing data from The Cancer Genome Atlas COAD, focusing on CRG expression patterns their clinicopathological correlations. Using Weighted Gene Co-expression Network Analysis (WGCNA) method, we identified gene module most strongly linked conducted functional enrichment analysis explore roles within this tumorigenesis. A prognostic risk model based four CRGs (ORC1, PTTG1, DLAT, PDHB) was developed stratify patients into high-risk low-risk groups, assessing overall survival, tumor microenvironment, mutational landscape differences. also evaluated therapeutic effects ferredoxin 1 (FDX1) elesclomol promoting HCT116 LoVo lines through various experiments, including proliferation, apoptosis assessment, mitochondrial membrane potential evaluation, DLAT lipoylation detection via Western blot. Certain showed different expressions versus normal tissues. WGCNA cuproptosis, crucial pathways like cycle regulation, citrate (TCA cycle), DNA replication. stratified high groups scores, revealing that had shorter survival distinct immune infiltration, while were more sensitive immunotherapy. Experimental results indicated FDX1 exerted an inhibitory effect its combination significantly reduced promoted apoptosis, increased lipoylation, lowered cells. findings study provided perspective research biomarkers strategies value patients, laid theoretical foundation future clinical application CRGs.

Language: Английский

Citations

0
MiRNA- 1293 Promotes Hepatocellular Carcinoma Cell Proliferation and Invasion by METTL3-Mediated m6 A Modification of Pri-miRNA- 1293 DOI
Jingwen Liu,

Beibe Zhu,

Nan Jin

et al.

Applied Biochemistry and Biotechnology, Journal Year: 2025, Volume and Issue: unknown

Published: April 28, 2025

Language: Английский

Citations

0
METTL3/IGF2BP1 influences the development of non‐small‐cell lung cancer by mediating m6A methylation modification of TRPV1 DOI Creative Commons

Wenjie Bai,

Gang Xiao,

Guijing Xie

et al.

Thoracic Cancer, Journal Year: 2024, Volume and Issue: 15(26), P. 1871 - 1881

Published: Aug. 1, 2024

Abstract Background Methyltransferase 3 (METTL3) accelerates N6‐methyladenosine (m6A) modifications and affects cancer progression, including non‐small‐cell lung (NSCLC). In this study, we aimed to explore the regulatory mechanisms of METTL3 underling NSCLC. Methods Immunohistochemical assay, quantitative real‐time polymerase chain reaction (qRT‐PCR) western blot assay were conducted for gene expression. MTT colony formation performed cell proliferation capacity. Cell apoptosis THP‐1 polarization estimated by flow cytometry analysis. migration invasion capacities evaluated transwell assay. Methylated RNA immunoprecipitation dual‐luciferase reporter actinomycin D treatment RIP analyze relationships METTL3, insulin‐like growth factor 2 mRNA binding protein 1 (IGF2BP1), transient receptor potential cation channel subfamily V member (TRPV1). The functions TRPV1 in vivo investigated through establishing murine xenograft model. Results expression was upregulated NSCLC related poor prognosis. silencing inhibited metastasis, induced apoptosis, repressed M2 macrophage polarization. results showed that IGF2BP1 could regulate m6A methylation modification. Moreover, deficiency growth, facilitated while overexpression restored impacts. addition, knockdown restrained tumor via regulating Conclusion bound enhanced IGF2BP1's recognition mRNA, thereby promoting inhibiting

Language: Английский

Citations

3
METTL3‐mediated the m6A modification of SF3B4 facilitates the development of non‐small cell lung cancer by enhancing LSM4 expression DOI Creative Commons

Guangsi He,

Kangsheng Gu, Jie Wei

et al.

Thoracic Cancer, Journal Year: 2024, Volume and Issue: 15(11), P. 919 - 928

Published: March 10, 2024

Abstract Background Splicing factor B subunit 4 (SF3B4) has been confirmed to participate in the progression of many cancers and is considered be a potential target for non‐small cell lung cancer (NSCLC). Thus, role molecular mechanism SF3B4 NSCLC deserves further study. Methods Quantitative real‐time PCR western blot were employed detect mRNA protein levels SF3B4, Sm‐like (LSM4) methyltransferase‐like 3 (METTL3). Cell proliferation, apoptosis, invasion, migration stemness tested by counting kit‐8, colony formation, flow cytometry, transwell, wound healing, sphere formation assays. The interaction between METTL3 or LSM4 was MeRIP, RIP Co‐IP Mice xenograft models constructed assess effects on tumorigenesis. Results had high expression tissues associated with shorter overall survival patients. Knockdown suppressed stemness, while inducing apoptosis. promoted stability m6A modification, its knockdown inhibited growth, metastasis downregulating SF3B4. could interact LSM4, sh‐SF3B4‐mediated inhibition functions reversed overexpression. In addition, reduced restrained tumor this effect Conclusion METTL3‐stablized via positively regulating LSM4.

Language: Английский

Citations

1