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Lactylation of METTL16 promotes cuproptosis via m6A-modification on FDX1 mRNA in gastric cancer

ABSTRACT: Lactylation of METTL16 promotes cuproptosis via m6A-modification on FDX1 mRNA in gastric cancer

PROVIDER: PRJNA932911 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23375755_1.fastq.gz	Fastqsanger.gz
	SRR23375755_2.fastq.gz	Fastqsanger.gz
	SRR23375756_1.fastq.gz	Fastqsanger.gz
	SRR23375756_2.fastq.gz	Fastqsanger.gz
	SRR23375757_1.fastq.gz	Fastqsanger.gz

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Lactylation of METTL16 promotes cuproptosis via m6A-modification on FDX1 mRNA in gastric cancer

Project description:To investigate the targets of METTL16-induced m6A modification, we established AGS lines in which METTL16 has been knocked down by shRNA.

2023-10-05 | GSE224890 | GEO

NUDT21 lactylation reprograms alternative polyadenylation to promote cuproptosis resistance

Project description:Alternative polyadenylation (APA) serves as a critical mechanism for shaping transcriptome diversity and modulating cancer therapeutic resistance. While lactate is a well-established metabolic signal in cancer progression, its role in APA regulation remains unclear. Here, we demonstrate that L-lactate-induced lactylation of NUDT21 drives transcriptomic reprogramming through APA modulation. NUDT21 lactylation enhances its interaction with CPSF6, facilitating CFIm complex formation and inducing 3′ untranslated region (UTR) lengthening of FDX1. Extension of the FDX1 3′ UTR attenuates its protein output, thereby conferring resistance to cuproptosis in esophageal squamous cell carcinoma (ESCC). Furthermore, we identify AARS1 as the lactylation “writer” catalyzing NUDT21 K23 lactylation, and HDAC2 as its enzymatic “eraser”. Clinically, elevated LDHA and NUDT21 levels correlate with reduced FDX1 expression and worse prognosis in ESCC patients. Notably, combined targeting of the lactate-NUDT21-FDX1-cuproptosis axis with the clinical LDHA inhibitor stiripentol and the copper ionophore elesclomol synergistically suppressed tumor growth. Collectively, our work identifies lactylated NUDT21 as a critical factor linking cellular metabolism to APA and proposes a promising therapeutic strategy for ESCC treatment.

2025-05-12 | GSE284372 | GEO

AKT1 confers tumor resistance to cuproptosis by phosphorylating FDX1

Project description:Cuproptosis, a recently defined copper-dependent cell death, remains largely unexplored in tumor therapies, particularly in breast cancer. Our study demonstrates that triple-negative breast cancer (TNBC) bears a relative elevated copper levels and exhibit resistance to cuproptosis. Mechanistically, cooper activates AKT1 signaling pathway, which inhibits cuproptosis by directly phosphorylating ferredoxin-1 (FDX1), a key regulator involved in cuproptosis. AKT1-mediated FDX1 phosphorylation abrogates FDX1-induced cuproptosis and aerobic respiration, accompanied by promoting glycolysis. Consequently, combination of AKT1 inhibitors MK2206 and the copper ionophore elesclomol (ES) synergistically inhibits TNBC tumorigenesis both in vitro and in vivo. In summary, our findings uncover a critical mechanism underlying TNBC resistance to cuproptosis and propose a potential therapeutic approach for TNBC.

2025-05-07 | PXD058176 | Pride

FDX1-mediated cuproptosis promotes cholestaic liver injury exacerbated by taurocholic acid

Project description:As the primary route for copper elimination, cholestasis raises questions about the role of copper in cholestatic liver injury and its specific molecular mechanisms. Our findings reveal that cholestasis-induced copper overload drives liver injury via taurocholic acid (TCA) -exacerbated and FDX1-mediated cuproptosis.

2026-01-14 | GSE300382 | GEO

Lactylation of METTL16 promotes cuproptosis via m<sup>6</sup>A-modification on FDX1 mRNA in gastric cancer.

Project description: Not available

| S-EPMC10589265 | biostudies-literature

SIRT5-Mediated FDX1 Desuccinylation Confers Cuproptosis Resistance in Lung cancer

Project description:Cuproptosis, a copper-dependent cell death process induced by excessive copper, represents an emerging therapeutic strategy in oncology. However, tumor specific molecular pathways regulating this process remain poorly defined. Here, we demonstrate that copper levels are elevated in lung adenocarcinoma (LUAD), and LUAD cell lines exhibit increased resistance to cuproptosis. Mechanistically，elevated copper stress promotes expression of the desuccinylase SIRT5 while reducing global succinylation in LUAD cells. Furthermore, we found that SIRT5 is a critical mediator of cuproptosis through the desuccinylation modification on Ferredoxin1(FDX1) protein at Lys84. This modification triggers TRIM8-mediated ubiquitination, leading to FDX1 proteasomal degradation and enhanced cuproptosis resistance. These results reveal the important role of SIRT5 in LUAD cuproptosis resistance. Notably, combining the SIRT5 inhibitor MC3482 with the cuproptosis inducer Elesclomol-Cu synergistically suppresses tumor growth in vitro and in

| PXD077292 |

FDX1-mediated cuproptosis promotes cholestaic liver injury exacerbated by taurocholic acid

Project description:FDX1-mediated cuproptosis promotes cholestaic liver injury exacerbated by taurocholic acid

| PRJNA1280175 | ENA

NUDT21 lactylation reprograms alternative polyadenylation to promote cuproptosis resistance

Project description:NUDT21 lactylation reprograms alternative polyadenylation to promote cuproptosis resistance

| PRJNA1198896 | ENA

Exploring the m6A modification profile after METTL16 overexpression in BEAS-2B cells.

Project description:Allergic asthma is a common disease. We aimed to investigate the role of METTL16, an N6-methyladenosine (m6A) writer, in allergic asthma and epithelial homeostasis. Here we show that pulmonary METTL16 expression was decreased in patients with allergic asthma and in a murine model of allergic asthma, particularly in airway epithelial cells. Genetic depletion of Mettl16 enhanced type 2 cytokine production and exacerbated epithelial-to-mesenchymal transition (EMT), whereas lung-specific METTL16 overexpression attenuated allergic airway inflammation and remodeling. Mechanistically, METTL16 promoted epithelial arginine biosynthesis and thereby suppressed IL-1β production. Furthermore, loss of Mettl16 impaired m6A modification of Ass1 mRNA, and increased Ass1 expression was associated with arginine biosynthesis. Our findings identify METTL16 as a critical regulator of allergic asthma and suggest it as a potential therapeutic target.

2026-08-04 | GSE341970 | GEO

Transcriptomic profiling of FDX1 knockdown in MOLM13 acute myeloid leukemia cells

Project description:RNA sequencing was performed to characterize transcriptomic changes associated with FDX1 depletion in acute myeloid leukemia cells. Stable FDX1-knockdown MOLM13 cells and corresponding negative-control MOLM13 cells were analyzed using three biologically independent replicates per group. The resulting dataset was used to identify gene-expression changes associated with FDX1 loss.

2026-08-18 | GSE343704 | GEO

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