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IGF2BP3 enhances ferroptosis resistance in colon cancer by stabilizing SLC7A11 mRNA and is regulated by miR-98-5p

ABSTRACT: IGF2BP3 enhances ferroptosis resistance in colon cancer by stabilizing SLC7A11 mRNA and is regulated by miR-98-5p

PROVIDER: PRJNA1224454 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32362963_1.fastq.gz	Fastqsanger.gz
	SRR32362963_2.fastq.gz	Fastqsanger.gz
	SRR32362964_1.fastq.gz	Fastqsanger.gz
	SRR32362964_2.fastq.gz	Fastqsanger.gz
	SRR32362965_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

IGF2BP3 enhances ferroptosis resistance in colon cancer by stabilizing SLC7A11 mRNA and is regulated by miR-98-5p

Project description:Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide, with increasing incidence and mortality rates. Resistance to cell death is a hallmark of cancer, and ferroptosis, a form of non-apoptotic cell death, has emerged as a critical factor in tumor suppression. The RNA-binding protein IGF2BP3, which plays a significant role in colon cancer progression, has been shown to modulate various oncogenic processes. However, its involvement in ferroptosis regulation in colon cancer remains largely unexplored. This study investigates the role of IGF2BP3 in ferroptosis regulation and its potential as a therapeutic target in colon cancer. Our data show that IGF2BP3 is upregulated in colon cancer tissues and correlates with poor prognosis. Knockdown of IGF2BP3 in colon cancer cell lines enhances sensitivity to ferroptosis induction, evidenced by increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels, which are reversed by the ferroptosis inhibitor ferrostatin-1. Mechanistically, IGF2BP3 regulates ferroptosis by stabilizing SLC7A11 mRNA, a key ferroptosis regulator, through its interaction with the mRNA. Additionally, miR-98-5p directly targets IGF2BP3, enhancing ferroptosis sensitivity. In vivo studies confirm that IGF2BP3 knockdown suppresses tumor growth, highlighting its potential as a therapeutic target. Overall, our findings suggest that IGF2BP3 plays a pivotal role in regulating ferroptosis in colon cancer, offering new avenues for therapeutic strategies in colon cancer treatment.

2025-02-21 | GSE289758 | GEO

The upregulation of miR-98-5p affects the glycosylation of IgA1 through cytokines in IgA nephropathy

Project description:Purpose: Increases in galactose-deficient IgA1 (Gd-IgA1) play a crucial role in the pathogenesis of IgA nephropathy (IgAN), and several recent experiments have shown that microRNAs (miRNAs) are involved in regulating the development and physiological function of the kidney. The aims of this study were to identify miRNAs that can affect the pathogenesis of IgAN and reveal the underlying regulatory mechanism of IgA1 glycosylation in peripheral blood Methods: The differentially expressed miRNAs in peripheral blood mononuclear cells (PBMCs) between IgAN patients and healthy controls were screened by high-throughput sequencing. The miRNA targets were predicted and verified by dual-luciferase reporter assays. We also explored the miRNA regulation of Gd-IgA1 through the transfection of miRNA mimics and related plasmids Results: The high-throughput sequencing results showed that miR-98-5p was highly expressed in the PBMCs of IgAN patients compared with healthy controls, and the luciferase reporter gene system confirmed that miR-98-5p might target chemokine ligand 3 (CCL3). The transfection of si-CCL3 confirmed that a decrease in CCL3 can affect the expression of interleukin-6 (IL-6) and C1GALT1. The overexpression of miR-98-5p in PBMCs via the transfection of miR-98-5p mimic reduced the CCL3 and C1GALT1 levels and increased the IL-6 levels. However, these changes in PBMCs were attenuated by cotransfection with the CCL3 plasmid. Conclusion: The results showed that miR-98-5p in PBMCs can target CCL3 to decrease its expression, which increased the IL-6 levels and the resulting increase in IL-6 can decrease C1GALT1 expression. Therefore, miR-98-5p might be involved in the development of IgAN.

2023-02-20 | GSE145652 | GEO

Extracellular vesicles-derived miR-760 and miR-98-5p as differentiating biomarkers for MS phenotypes

Project description:Objective. Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system with heterogenous clinical course, lacking non-invasive biomarkers for early phenotype differentiation. This study aimed to identi-fy circulating extracellular vesicle (EV)-derived miRNA signatures and as-sociated disease-specific molecular markers capable of distinguishing stable relapsing-remitting MS (RRMS) from secondary progressive MS (SPMS). Materials and methods. Plasma samples were collected from patients with stable RRMS, SPMS, and healthy controls (HC), followed by EVs isolation and characterization using transmission electron microscopy, dynamic light scattering, and flow cytometry. RNA was extracted from EVs, and miRNA profiles were ana-lyzed via RNA sequencing and RT-qPCR. Cytokine and neurodegeneration marker levels were quantified using the BioPlex® multiplex system and ELISA. Functional enrichment and network analyses of miRNA targets were performed, alongside logistic regression modeling to assess diagnostic utility. Results. Four EV-derived miRNAs (miR-760, miR-98-5p, miR-301a-3p, and miR-223-3p) showed significant differences between stable RRMS and SPMS. The integrative model incorporating these miRNAs with FGF basic protein achieved excellent discrimination between MS phenotypes (AUC = 0.97). Moreover, miR-760 emerged as the most robust predictive biomarker for stable RRMS classification. In turn, miR-98-5p showed the highest up-regulation in both stable RRMS and SPMS relative to HC. miRNA targets network analysis further revealed distinct immunoregulatory patterns for stable RRMS and SPMS. Conclusions. Plasma-derived EV-miRNAs, particularly miR-760 and miR-98-5p, showed strong potential as non-invasive biomarkers for stable RRMS and SPMS phenotypes. Integrating EV-miRNA profiling with protein bi-omarkers enhances diagnostic precision and may support personalized management strategies in MS.

2026-02-11 | GSE303912 | GEO

IGF2BP3 promotes progression of head and neck cancers through the circHECTD2/hsa_miR_4310/7157-5p/Smad2 signaling axis in an m6A modification–dependent manner

Project description:Accumulating evidence indicates that N6-methyladenosine (m6A) modification of circular RNAs (circRNAs) plays a pivotal role in regulating cancer progression. However, in head and neck squamous cell carcinoma (HNSCC), the biological functions and underlying mechanisms of m6A modification in circRNAs remain insufficiently elucidated. In this study, we demonstrated that IGF2BP3, an upstream m6A reader, is associated with poor clinical outcomes. IGF2BP3 stabilizes circHECTD2 through binding, and m6A modification enhances this interaction. Mechanistic investigations revealed that IGF2BP3 binds to and stabilizes circHECTD2, which functions as a sponge for hsa-miR-4310 and hsa-miR-7157-5p, thereby preventing the degradation of SMAD2 mRNA and promoting tumor proliferation, invasion, and metastasis in HNSCC. Collectively, these findings suggest that IGF2BP3 and circHECTD2 may serve as promising prognostic biomarkers and therapeutic targets for HNSCC.

2026-04-15 | GSE313611 | GEO

IGF2BP3 controls cancer cell invasiveness by modulation RISC function

Project description:The goal of this study was to determine IGF2BP3 regulation of RNA targets in human pacreatic ductal adenocarcinoma cell lines Included are iCLIP-seq libraries for IGF2BP3 from PL45 and Panc1 PDAC cell samples, RIP-seq samples from PL45 and Panc1 PDAC cells, RNA-seq data sets from control and IGF2BP3 knockdown in PL45 and Panc1 PDAC cells, and small RNA-seq samples from Panc1 cells

2016-03-12 | E-GEOD-79147 | biostudies-arrayexpress

The Deubiquitylase USP52 Regulates Cell Proliferation and Ferroptosis through Stabilizing SLC7A11/xCT in Bladder Cancer

Project description:The Deubiquitylase USP52 Regulates Cell Proliferation and Ferroptosis through Stabilizing SLC7A11/xCT in Bladder Cancer

| PRJNA1095871 | ENA

The RNA binding protein IGF2BP3 promotes hematopoietic progenitor cell proliferation by targeting leukemogenic pathways

Project description:The goal of this study was to determine IGF2BP3 RNA targets in human B-cell Acute Lymphocitic Leukemia cell models. Included are iCLIP-seq libraries for IGF2BP3 from RS4;11 and REH B-ALL cell samples and RNA-seq data sets from control and IGF2BP3 knockdown RS4;11 B-ALL cell lines

2016-01-16 | E-GEOD-76931 | biostudies-arrayexpress

Panicum sp. 98 strain:98 | cultivar:98

Project description:Panicum sp. 98 Transcriptome - 98 RT

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IGF2BP3 Inhibits Translation in Round Spermatozoa

Project description:To reveal the effects of IGF2BP3 on mouse spermatids at the post-transcriptional and translational levels, we performed RNA-seq and ribosome nascent-chain complex sequencing (RNC-seq) of spermatids from Igf2bp3+/- and Igf2bp3-/- mice after isolation. RNA-seq and RNC-seq sequencing showed that IGF2BP3 mainly plays a regulatory role in translational repression in spermatids.

2025-11-30 | GSE256054 | GEO

Let-7, mir-98 and mir-181 as biomarkers for cancer and schizophrenia

Project description:Recent evidence supports a role of microRNAs in cancer and psychiatric disorders such as schizophrenia and bipolar disorder, through their regulatory role on the expression of multiple genes. The rather rare co-morbidity of cancer and schizophrenia is an old hypothesis which needs further research on microRNAs as molecules that might exert their oncosuppressive or oncogenic activity in the context of their role in psychiatric disorders The expression pattern of a variety of different microRNAs was investigated in patients (N=6) suffering from schizophrenia termed control, patients with a solid tumor (N=10) and patients with both schizophrenia and tumor (N=8). miRNA profiling was performed on whole blood samples using the miRCURY LNA™ microRNA Array technology (6th & 7th generation). Significant down-regulation of the let-7p-5p, miR-98-5p and of miR-183-5p in the study groups (tumor alone and tumor and schizophrenia) was observed (p<0.05). let-7, miR-98 and miR-183 may play an important oncosuppressive role through their regulatory impact in gene expression irrespective of the presence of schizophrenia

2015-01-22 | GSE65143 | GEO

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