Medical Oncology, Год журнала: 2025, Номер 42(3)
Опубликована: Янв. 24, 2025
Язык: Английский
Medical Oncology, Год журнала: 2025, Номер 42(3)
Опубликована: Янв. 24, 2025
Язык: Английский
Biology Direct, Год журнала: 2023, Номер 18(1)
Опубликована: Сен. 1, 2023
Hepatocellular carcinoma (HCC) is one of the most common and challenging cancers in world. N6-methyladenosine (m6A) modification long non-coding RNAs (lncRNAs) play critical roles progression HCC. However, there are few reports on genome-wide screening functional annotations m6A-methylated lncRNAs HCC.The expression levels m6A methyltransferase METTL3 association with prognosis HCC were determined by RT-qPCR, public dataset platforms. Then, RNA-seq, Pearson correlation analysis, MeRIP-qPCR, RNA half-life assay, gene site-directed mutation, RIP assay RT-qPCR analysis employed to determine downstream target Subsequently, lncRNA glucosylceramidase beta pseudogene 1 (GBAP1) Kaplan-meier curves, vitro experiments vivo tumorigenesis lung metastasis models. pathway GBAP1 explored GO biological process, KEGG enrichment, luciferase reporter rescue so on.METTL3 was upregulated closely related prognosis. And induced acting as writer IGF2BP2 worked its reader. Clinically, significantly associated tumor size, venous infiltration, TNM stage HCC, Functionally, promoted growth both vivo. Furthermore, acted molecular sponge for miR-22-3p increase bone morphogenetic protein receptor type 1A (BMPR1A), which then activated BMP/SMAD cells.Our findings demonstrated that METTL3-induced migration, invasion proliferation cells via GBAP1/miR-22-3p/BMPR1A/SMAD axis. could be a potential indicator therapeutic
Язык: Английский
Процитировано
21Translational Lung Cancer Research, Год журнала: 2024, Номер 13(5), С. 1121 - 1136
Опубликована: Май 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.
Язык: Английский
Процитировано
7Molecular Cancer, Год журнала: 2024, Номер 23(1)
Опубликована: Май 31, 2024
Elevated evidence suggests that the SENPs family plays an important role in tumor progression. However, of AML remains unclear.
Язык: Английский
Процитировано
7Oncogene, Год журнала: 2024, Номер 43(34), С. 2548 - 2563
Опубликована: Июль 16, 2024
Язык: Английский
Процитировано
7Experimental Hematology and Oncology, Год журнала: 2024, Номер 13(1)
Опубликована: Янв. 24, 2024
Abstract Background t(8;21)(q22;q22) is one of the most frequent chromosomal abnormalities in acute myeloid leukemia (AML), leading to generation fusion protein AML1-ETO. Despite t(8;21) AML being considered as a subtype with favorable prognosis, approximately 30–50% patients experience drug resistance and subsequent relapse. N 6 -methyladenosine (m A) demonstrated be involved development AML. However, regulatory mechanisms between AML1-ETO m A-related enzymes roles dysregulated A modifications t(8;21)-leukemogenesis chemoresistance remain elusive. Methods Chromatin immunoprecipitation, dual-luciferase reporter assay, A-qPCR, RNA stability assay were used investigate loop FTO, an demethylase. Gain- loss-of-function experiments both vitro vivo further performed. Transcriptome-wide sequencing conducted identify potential targets FTO. Results Here we show that FTO highly expressed AML, especially primary refractory disease. The expression positively correlated AML1-ETO, which attributed positive Mechanistically, upregulates through inhibiting transcriptional repression mediated by PU.1. Meanwhile, promotes YTHDF2-mediated mRNA decay. Inactivation significantly suppresses cell proliferation, differentiation renders resistant cells sensitive Ara-C. exerts functions regulating its targets, IGFBP2, A-dependent manner. Regain Ara-C tolerance observed when IGFBP2 overexpressed FTO-knockdown cells. Conclusion Our work reveals therapeutic targeting AML1-ETO/FTO/IGFBP2 minicircuitry treatment for
Язык: Английский
Процитировано
6Journal of Translational Medicine, Год журнала: 2024, Номер 22(1)
Опубликована: Фев. 14, 2024
Abstract Skeletal system disease (SSD) is defined as a class of chronic disorders skeletal with poor prognosis and causes heavy economic burden. m6A, methylation at the N6 position adenosine in RNA, reversible dynamic modification posttranscriptional mRNA. Evidences suggest that m6A modifications play crucial role regulating biological processes all kinds diseases, such malignancy. Recently studies have revealed most abundant epigentic modification, involved progression SSD. However, function SSD not fully illustrated. Therefore, make clear relationship between pathogenesis might provide novel sights for prevention targeted treatment This article will summarize recent advances regulation SSD, including osteoporosis, osteosarcoma, rheumatoid arthritis osteoarthritis, discuss potential clinical value, research challenge future prospect
Язык: Английский
Процитировано
5Cancer Science, Год журнала: 2024, Номер 115(7), С. 2360 - 2370
Опубликована: Апрель 24, 2024
N6-methyladenosine (m6A) is an RNA modification involved in processing and widely found transcripts. In cancer cells, m6A upregulated, contributing to their malignant transformation. this study, we analyzed gene expression tissues, ducts, acinar cells derived from pancreatic patients using MeRIP-seq. We that dozens of RNAs highly modified by were detected tissues compared with ducts cells. Among them, the m6A-activated mRNA TCEAL8 was observed, for first time, as a potential marker cancer. Spatially resolved transcriptomic analysis showed expressed specific activation cancer-related signaling pathways observed relative TCEAL8-negative Furthermore, among TCEAL8-positive expressing m6A-modifying enzyme METTL3 co-activation Notch mTOR signaling, also known be metastasis. Overall, these results suggest novel transformation
Язык: Английский
Процитировано
5Toxicology, Год журнала: 2024, Номер 503, С. 153758 - 153758
Опубликована: Фев. 16, 2024
Язык: Английский
Процитировано
4Journal of Translational Medicine, Год журнала: 2024, Номер 22(1)
Опубликована: Май 24, 2024
Abstract N6-methyladenosine (m6A) stands as the most prevalent modified form of RNA in eukaryotes, pivotal various biological processes such regulating stability, translation, and transcription. All members within YT521-B homology (YTH) gene family are categorized m6A reading proteins, capable identifying binding modifications on RNA, thereby metabolism functioning across diverse physiological processes. YTH domain-containing 2 (YTHDC2), identified latest member family, has only recently started to emerge for its function. Numerous studies have underscored significance YTHDC2 human physiology, highlighting involvement both tumor progression non-tumor diseases. Consequently, this review aims further elucidate pathological mechanisms by summarizing functions roles tumors other diseases, with a particular focus downstream molecular targets signaling pathways.
Язык: Английский
Процитировано
4Molecular Biomedicine, Год журнала: 2024, Номер 5(1)
Опубликована: Авг. 19, 2024
Abstract Transcription, RNA splicing, translation, and post-translational protein modification are fundamental processes of gene expression. Epigenetic modifications, such as DNA methylation, play a crucial role in regulating The methyltransferase-like (METTL) family, constituent the 7-β-strand (7BS) methyltransferase subfamily, is broadly distributed across cell nucleus, cytoplasm, mitochondria. Members METTL through their S-adenosyl methionine (SAM) binding domain, can transfer methyl groups to DNA, RNA, or proteins, thereby impacting replication, transcription, mRNA participate maintenance normal function promote disease development. This review primarily examines involvement family differentiation, mitochondrial function, its association with tumor formation, nervous system, cardiovascular diseases. Notably, intricately linked cellular particularly regulation translation factors. represent important molecules development associated patient immunity tolerance radiotherapy chemotherapy. Moreover, future research directions could include drugs antibodies targeting structural domains, utilizing nanomaterials carry miRNA corresponding mRNA. Additionally, precise mechanisms underlying interactions between factors remain be clarified.
Язык: Английский
Процитировано
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