Ask about this productRelated genes to: IRX3 Blocking Peptide
- 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 Blocking Peptide
Related articles to: IRX3 Blocking Peptide
- Adipocytes play a critical role in the breast cancer tumorigenic microenvironment. However, their effects and underlying mechanisms remain unclear. This study aims to investigate the role of adipocytes in luminal A breast cancer invasiveness at the cellular and molecular levels. Various adipocyte types were co-cultured with MCF7 breast cancer cells in direct and indirect manners. Invasiveness was assessed via proliferation, migration, and invasion, with alterations examined at morphological, cellular, and molecular levels. The role of adipocytes on MCF7 was further explored using an orthotopic breast cancer xenograft mouse model. MCF7 co-cultured with adipocytes, especially brown adipocytes (BAC), showed increased invasiveness and tumorigenic potential. Morphologically, co-cultivation with BAC increased the proliferation, EMT, and stemness of MCF7. Mechanistically, co-culture of MCF7 with BAC exhibited disturbed expression of genes related to adipogenesis and mitochondrial dynamics; notably, IRX3 was the most prominently elevated one. Knockdown of IRX3 restored balanced mitochondrial function and reduced both the invasiveness of breast cancer cells in vitro and tumor growth in vivo. Brown adipocytes promote breast cancer invasiveness by upregulating adipogenesis-related IRX3, which acts via the mitochondrial functional regulation. - Source: PubMed
Publication date: 2026/05/22
Hu ShihangHu BinSu ShiqiongZhou YingLiu GangGao YuzheNi QingHou Jing - Generating mature human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) remains a major obstacle to accurate disease modeling and cardiac repair. As the transcription factor Irx3 is a key determinant of ventricular conduction system fate in mice, we hypothesized that suppressing IRX3 expression accelerates human working cardiomyocyte differentiation. Here, we demonstrate that depleting IRX3 enhances hiPSC-CM differentiation. IRX3-knockout (KO) hiPSCs generated a greater number of cardiomyocytes with elevated expression of TNNI1 and CX43. Notably, IRX3-KO cardiomyocytes exhibited improved electrophysiological properties, more uniform mitochondrial distribution, better sarcomere organization, and enhanced intercellular connectivity. We observed that IRX3 expression peaks during the early stages of cardiomyocyte differentiation, whereas IRX3-KO cardiac progenitors have increased expression of GATA4, NKX2-5, and TBX5, as well as enhanced cell proliferation. These integrative analyses indicate that IRX3 influences cardiomyocyte differentiation by modulating the gene regulatory networks driven by GATA4, NKX2-5, and TBX5, providing functional evidence linking gene regulatory networks to the structural and electrophysiological development of cardiomyocytes. Collectively, these findings identify IRX3 as a key regulator of early cardiac commitment and highlight the potential of IRX3 suppression to enhance the molecular and functional phenotype of hiPSC-derived cardiomyocytes. - Source: PubMed
Publication date: 2026/06/16
Ribeiro Kalthof AgathaFerreira Nikolas DreschSilva Caio MateusCordeiro Valadão IuriPinheiro de Sousa IguaracyBertoldi Ester Riserio MatosLima Vanessa MoraisTuraca Lauro ThiagoBarbosa Ana Beatriz Ruiz AfonsoFonseca-Alaniz Miriam HelenaConcordet Jean-PaulNeri Elida AdalgisaKrieger Jose E - 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