Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

M6A reader IGF2BP3 promotes endometrial cancer progression through modification circ-EPB41L2

ABSTRACT: Endometrial cancer ranks as the primary contributor to cancer related fatalities on a global scale. IGF2BP3 is a reader protein of m6A modification and plays an important role in the carcinogenesis of many solid tumors. Here, we explored the role and underlying mechanism of IGF2BP3 on endometrial cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE333959 | GEO | 2026/06/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression

2025-05-01 | GSE202026 | GEO

RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression (MeRIP-Seq)

Project description:Triple-negative breast cancer (TNBC) is a group of fatal malignancies characterized by high metastatic capacity, the underlying mechanisms of which remain largely elusive. We found here that insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3), but not other members of the IGF2BP family, is highly expressed in breast cancer and correlated clinically with TNBC metastasis and patient prognosis. IGF2BP3 promotes the migration and invasion capabilities of TNBC cells dependent upon cellular RNA N6-methyladenosine (m6A) modification. Mechanistically, IGF2BP3 binds to and unstabilizes m6A-methylated mRNA of the extracellular matrix glycoprotein, SLIT2, impairs its downstream signaling via the cognate receptor ROBO1, and consequently derepresses the canonical oncogenic PI3K/AKT and MEK/ERK pathways. These findings shed light into the regulatory network of distal metastasis and provide rationale for targeting the m6A machinery in the treatment of TNBC

2025-05-03 | GSE202235 | 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

Potential Roles of IGF2BP3 in Bladder Cancer [m6A-seq]

Project description:TCGA data analysis and clinical sample test results showed the IGF2BP3 is highly expressed in bladder cancer and related to tumor metastasis and invasion. RNA sequencing results of clinical bladder tissue from 53 cases showed that the IGF2BP3 expression is related to cell proliferation genes. M6a and RNA sequencing results showed the IGF2BP3 affects the growth, proliferation, and apoptosis of T24 cells, and SpHK1, POMT2, and MRPS18a may be potential targets of IGF2BP3.

2024-03-27 | GSE171023 | GEO

Potential Roles of IGF2BP3 in Bladder Cancer [RNA-Seq]

2024-03-27 | GSE171022 | GEO

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

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

IGF2BP3 Regulates Expression and Alternative Splicing of Genes associated with the Progression of Gastric Cancer in AGS cells

Project description:Gastric cancer has become the fifth largest malignant tumor in the world, with a mortality rate ranking fourth. IGF2BP3, as a multifunctional RNA binding protein, is involved in regulating alternative splicing and m6A modification. Research has shown that IGF2BP3 plays a carcinogenic role in the development of gastric tumors. However, there is currently relatively little research on the impact of IGF2BP3 as an RNA binding protein (RBP) on alternative splicing in gastric cancer cells. The specific function of IGF2BP3 as an RBP and its molecular mechanisms involved in the development and progression of gastric cancer are still unclear. The aim of this study is to explore the mechanism by which IGF2BP3 affects gene expression and alternative splicing by binding to mRNA, and thus plays a role in the development of gastric cancer cells. We overexpressed IGF2BP3 in gastric cancer cells (AGS) and obtained transcriptome data (RNA seq) on the effects of IGF2BP3 using high-throughput transcriptome sequencing. We then analyzed potential targets in AGS cells where transcription and alternative splicing levels are regulated by IGF2BP3, and explored the molecular mechanisms by which IGF2BP3 affects gene expression and alternative splicing in AGS cells.

2025-03-05 | GSE276928 | GEO

IGF2BP3 promotes mRNA degradation through internal m7G modification [seq_Ribo]

Project description:Recent studies have suggested that mRNA internal m7G and its writer protein METTL1 are closely related to cell metabolism and cancer regulation. Here, we identify that IGF2BP family proteins IGF2BP1-3 can preferentially bind internal mRNA m7G. Such interactions, especially IGF2BP3 with m7G, could promote the degradation of m7G target transcripts in cancer cells. IGF2BP3 is more responsive to changes of the m7G modification, while IGF2BP1 prefers m6A to stabilize the bound transcripts. We also demonstrate that p53 transcript, TP53, is m7G-modified at its 3’UTR in cancer cells. In glioblastoma, the methylation level and the half lifetime of the modified transcript could be modulated by tuning IGF2BP3, or by site-specific targeting of m7G through a dCas13b-guided system, resulting in modulation of cancer progression and chemosensitivity.

2024-07-15 | GSE269962 | GEO

IGF2BP3 promotes mRNA degradation through internal m7G modification [PARCLIP]

2024-07-15 | GSE266130 | GEO