Ask about this productRelated genes to: EIF4A3 antibody
- Gene:
- EIF4A3 NIH gene
- Name:
- eukaryotic translation initiation factor 4A3
- Previous symbol:
- DDX48
- Synonyms:
- KIAA0111, EIF4AIII, Fal1
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2019-04-23
Related products to: EIF4A3 antibody
Related articles to: EIF4A3 antibody
- Liver metastasis is a major cause of mortality in gastric cancer (GC), yet the underlying molecular mechanisms remain poorly understood. Long non-coding RNAs (lncRNAs) have emerged as key regulators of gene expression and cancer progression, but their roles in GC liver metastasis are not fully defined. In this study, lncRNA sequencing of primary GC tumors and matched liver metastatic tissues identified PSPC1-AS2 as significantly upregulated. Its elevated expression was further validated across multiple patient cohorts and public datasets. Functional assays demonstrated that PSPC1-AS2 promotes GC cell migration, invasion, and liver metastasis both in vitro and in vivo. Mechanistically, PSPC1-AS2 is predominantly localized in the nucleus and enhances the mRNA stability of its neighboring gene PSPC1 by recruiting the RNA-binding protein EIF4A3. The PSPC1-AS2/PSPC1 axis facilitates tumor progression and induces macrophage polarization toward the pro-tumorigenic M2 phenotype via increased CCL2 secretion. At the molecular level, PSPC1 interacts with PARP1, competitively inhibiting PARP1-mediated PARylation and dephosphorylation of STAT3, thereby sustaining STAT3 activation and promoting CCL2 transcription. Notably, neutralization of CCL2 effectively reverses PSPC1-induced M2 macrophage polarization. Collectively, these findings reveal a novel PSPC1-AS2/PSPC1/STAT3/CCL2 regulatory axis that drives GC progression and liver metastasis through remodeling of the tumor microenvironment, highlighting a potential therapeutic target for advanced gastric cancer. - Source: PubMed
Publication date: 2026/04/15
Zhong YuejiaoZhou XuemeiZhou YuanShi HaozeMo SuoHuang YutingCheng XianfengChen HaoYin Li - Gastric cancer (GC) is characterized by high mortality due to late-stage diagnosis and aggressive metastatic behavior. Epithelial-mesenchymal transition (EMT), primarily driven by the TGF-β/SMAD signaling, critically contributes to GC progression. However, the molecular mechanisms regulating this pathway remain incompletely understood. - Source: PubMed
Publication date: 2026/04/10
Liu YujingZhang YanhuaDou WenhuanPeng WeiCheng MingZhou YanShao QiankunWu Yongyou - - Source: PubMed
Publication date: 2026/04/05
Meng FanZhang XiaokangWang XinlinQiu BinqiangZeng DingchengHuang XiaoLiu JianpingWu HaiwuCui KaiwangZhong BinLiu WeiyouGong XiangwenHe Xin - Macrophage-driven inflammation is central to the pathogenesis of sepsis-induced acute kidney injury (SI-AKI), yet the role of RNA-binding proteins (RBPs) in post-transcriptionally regulating this process remains elusive. Here, we identify the RBP zinc finger X-linked duplicated B (ZXDB) as an upstream contributor to SI-AKI by promoting a pathogenic, pro-inflammatory macrophage activation state. We found that ZXDB expression is consistently elevated in M1-like macrophages within the kidney during SI-AKI, where it stimulates pro-inflammatory cytokine secretion and glycolytic reprogramming. Mechanistically, we discovered that ZXDB directly interacts with EIF4A3, a core exon junction complex (EJC) DEAD-box RNA helicase, via its aa151-300 region, thereby enhancing ACACA 5'UTR-dependent translation of ACACA, a metabolic enzyme that mediates downstream pathogenic effects associated with ZXDB activation. Critically, macrophage-specific deletion of Zxdb attenuated disease severity in a mouse model of SI-AKI, preserving renal function and attenuating inflammation. Taken together, our study uncovers a novel ZXDB-EIF4A3-ACACA axis that orchestrates macrophage-mediated kidney injury through translational control of metabolism, thereby suggesting ZXDB as a potential therapeutic candidate for SI-AKI. - Source: PubMed
Wu HaiyangGang WeiWang LiSun JingLi ShuangxiGuo Zhiyong - Selenoproteins are critical regulators of redox homeostasis, protein folding, and metabolism, and their dysregulation has been implicated in cancer biology. Among them, selenoprotein F (SELENOF) has been reported to be tumor suppressive, whereas the RNA-binding protein EIF4A3, a component of the exon junction complex, has been implicated in post-transcriptional repression of selenoproteins. The regulatory and clinical significance of this interaction in colorectal adenocarcinoma (COAD) remains unclear. We performed an integrative analysis of transcriptomic data from The Cancer Genome Atlas (TCGA), proteomic data from the Clinical Proteomic Tumor Analysis Consortium (CPTAC), and patient tissue microarrays. Western blotting, qRT-PCR, and immunofluorescence staining were used to examine SELENOF, GPX1, and EIF4A3 expression in colon cancer cell lines and tumor tissues. Correlation, regression, and survival analyses were conducted, and pathway enrichment was assessed using gene set enrichment analysis (GSEA) of RNA and proteome correlation profiles. Motif discovery and translational efficiency analyses were performed to identify 3'-UTR features associated with EIF4A3 repressive activity. SELENOF and EIF4A3 showed inverse, stage-dependent protein expression patterns in COAD in the CPTAC cohort. Survival analyses demonstrated that SELENOF alone was not prognostic but acquired significance in EIF4A3-high tumors, where low SELENOF was associated with poor outcomes. Motif analyses identified enriched 3'UTR elements in SELENOF, suggesting that EIF4A3 represses translation through non-SECIS motifs positioned near canonical SECIS elements. Our findings explore a novel EIF4A3-SELENOF regulatory axis in colorectal cancer. SELENOF acquires conditional prognostic significance only in the context of elevated EIF4A3, highlighting the importance of molecular interaction specificity in biomarker discovery. - Source: PubMed
Publication date: 2026/03/19
Shaheed AvneetMehta ShriyaSverdlov MariaDeaton RyanKastrati IridaPhoenix John TKregel StevenDiamond Alan MBera Soumen