Ask about this productRelated genes to: IRX3 antibody
- Gene:
- IRX3 NIH gene
- Name:
- iroquois homeobox 3
- Previous symbol:
- -
- Synonyms:
- IRX-1
- Chromosome:
- 16q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-27
- Date modifiied:
- 2015-08-25
Related products to: IRX3 antibody
Related articles to: IRX3 antibody
- Vascular injury triggers perivascular adipose tissue (PVAT) browning, an adaptive response critical for vascular protection, yet its regulatory mechanisms remain unclear. This study aimed to identify key pathways governing PVAT browning and evaluate their therapeutic potential in vascular repair. - Source: PubMed
Publication date: 2026/05/14
Hu XiaoyongLi HongjianYang ZhaoyingLv ZhongyingZhang YingZou TingTang RuiZhang QiuyuAbudula AdiliMalasadi Nuhanguli - Hepatocellular carcinoma (HCC) shows a marked predominance in men, yet the molecular basis for this sex disparity remains unclear. The present study leveraged multi-omics data and machine learning algorithms to identify key genes associated with sex-specific differences in HCC and to screen for putative candidate compounds, aiming to provide new insights for sex-specific therapy. The mRNA expression data of male and female patients with HCC and paracancerous tissues were obtained from the GEO and TCGA databases. To mitigate overfitting, data were partitioned into independent training and testing sets. Candidate genes were screened by differential expression analysis and weighted gene co-expression network analysis. A total of four complementary algorithms, random forest, support vector machines, generalized linear models and extreme gradient boosting were used to identify key genes with high predictive capability. CYP17A1 and IRX3 were identified as the top differentially expressed core genes associated with HCC in men. Pan-cancer analysis showed that CYP17A1 was lowly expressed in the majority of tumors, but significantly highly expressed in HCC, rectal adenocarcinoma and gastric cancer (P<0.001). Functional cell-based assays showed that knockout of CYP17A1 inhibited the proliferation, migration and invasion ability of HCC cells (P<0.001). Immunohistochemistry showed that CYP17A1 protein expression was significantly increased in HCC tissues from male patients when compared with that in paracancerous tissues (P<0.001), whereas there was no significant difference in female patient tissues (P>0.05). Notably, while IRX3 was identified computationally, its functional role remains to be experimentally validated. Molecular docking predicted a potential interaction between the natural compound Saikosaponin A and the CYP17A1 protein, and cellular assays revealed that it dose-dependently inhibits HCC cell malignant phenotypes. The present study suggests that CYP17A1 is associated with sex differences in HCC, potentially via the androgen signaling axis. Furthermore, IRX3 emerges as a novel hypothesis-generating candidate gene. Finally, the findings of the present study highlight Saikosaponin A as a putative therapeutic candidate for male patients with HCC, warranting further target-dependency investigations. - Source: PubMed
Publication date: 2026/04/24
Wang ZhenNing JinghuaZhang HongyuanRuan QingfenZhao YanhongQu RunLv CongcongWu YutongLiu WeidongYang XiaoyinLi ZimingLiang YiZhang Yuzhe - Dimethyl sulfoxide can be used to promote mature hepatocyte-like differentiation in hepatocellular carcinoma cells and sustain the expression of liver-specific genes, which is considered a potential novel therapy for liver cancer treatment. However, the molecular targets of dimethyl sulfoxide, especially transcription factors, remain largely unknown. In this study, we show that dimethyl sulfoxide treatment significantly downregulates Iroquois-homeobox protein 3 in Hepatocellular carcinoma cells, illustrating that Iroquois-homeobox protein 3 might regulate Hepatocellular carcinoma proliferation positively. Further clinical data reveal that Iroquois-homeobox protein 3 expression is generally elevated in human Hepatocellular carcinoma tissues and correlates with poor patient survival. Consistent with these observations, gain- and loss-of-function studies demonstrate that Iroquois-homeobox protein 3 promotes Hepatocellular carcinoma proliferation both in vitro and in vivo. Mechanistically, Iroquois-homeobox protein 3 binds to the promoter of F2R-like trypsin receptor 1/Protease-Activated Receptor 2, recruits RNA polymerase II and increases Serine 5 phosphorylation of its C-terminal domain (CTD), thereby upregulating F2R-like trypsin receptor 1/Protease-Activated Receptor 2 expression and driving Hepatocellular carcinoma proliferation. Collectively, our findings reveal a critical role for Iroquois-homeobox protein 3 in Hepatocellular carcinoma development and suggest that Iroquois-homeobox protein 3 might be a potential therapeutic target for Hepatocellular carcinoma. - Source: PubMed
Publication date: 2026/05/07
Yang LijuanHuo ZiyeQian XinRen YiLan XiangFan Hui - A major challenge in deciphering the complex genetic landscape of polycystic ovary syndrome (PCOS) lies in the limited understanding of how susceptibility loci drive molecular mechanisms across diverse phenotypes. To address this, we integrated molecular and epigenomic annotations from proposed causal cell types and employed a deep learning (DL) framework to predict cell type-specific regulatory effects of PCOS-risk variants. Our analysis revealed that these variants affect key transcription factor-binding sites, including , , , and , which regulate gonadotropin signaling, folliculogenesis, and steroidogenesis across brain and endocrine cell types. The DL model, which showed strong concordance with reporter assay data, identified enhancer-disrupting activity in ∼20% of risk variants. Notably, many of these variants disrupt transcription factors involved in androgen-mediated signaling, providing molecular insights into hyperandrogenemia in PCOS. Variants prioritized by the model were more pleiotropic and exerted stronger regulatory effects on gene expression compared with other risk variants. Using the locus as a case study, we demonstrate how regulatory disruptions in tissues such as the fetal brain, pancreas, adipocytes, and endothelial cells may link obesity-associated mechanisms to PCOS pathogenesis via neuronal development, metabolic dysfunction, and impaired folliculogenesis. Collectively, our findings highlight the utility of integrating DL models with epigenomic data to uncover disease-relevant variants, reveal cross-tissue regulatory effects, and refine mechanistic understanding of PCOS. - Source: PubMed
Publication date: 2026/04/09
Srivastava JayaOvcharenko Ivan - The Iroquois () family of homeobox genes regulates critical developmental processes, and emerging evidence suggests that their dysregulation contributes to cancer progression, particularly in relation to cancer stemness. Although their expression appears to be influenced by hormonal regulation, their potential roles in hormone-sensitive cancers remain incompletely understood. In this study, we performed a comprehensive, exploratory analysis of all six Iroquois genes (-) across prostate, breast, ovarian, and endometrial cancers. Using large-scale publicly available transcriptomic datasets, we systematically examined gene expression patterns and their associations with tumour progression, prognosis, hormone regulation, drug response, and cancer stemness. and were consistently elevated in estrogen-dependent tumours and 2 and 4 were notably upregulated in prostate cancer. Despite evidence of estrogen receptor 1 (ESR1) and androgen receptor (AR) binding near several promoters, estrogen treatment assays showed that ESR1 binding at promoters alone was insufficient to induce transcription. Clinically, 2 expression was associated with favourable outcomes in breast, endometrial, and ovarian cancers and showed correlations with stemness-related signatures in prostate cancer. Similarly, 4 expression was associated with stemness features in prostate and endometrial cancers. In addition, 6 expression showed associations with reduced sensitivity to abiraterone, suggesting a potential link with therapeutic resistance in these tumours. Collectively, these findings highlight the context-dependent expression patterns and clinical associations of genes across hormone-driven cancers. While largely correlative, this study provides a framework for future functional investigations and suggests that selected s may have potential utility as biomarkers for disease stratification and treatment response in hormone-sensitive cancers. - Source: PubMed
Publication date: 2026/02/24
Thennakoon AmaliFernando AchalaBatra Jyotsna