Ask about this productRelated genes to: FJX1 antibody
- Gene:
- FJX1 NIH gene
- Name:
- four-jointed box kinase 1
- Previous symbol:
- -
- Synonyms:
- FLJ22416, FLJ25593
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2018-09-27
Related products to: FJX1 antibody
Related articles to: FJX1 antibody
- Focused ultrasound, low-intensity focused ultrasound, and microbubble-enhanced sonoporation are examples of ultrasound-based cancer therapies that have shown promise as biophysical modalities for enhancing drug penetration, immunogenic cell death, and targeted delivery of radiopharmaceuticals in solid tumors. The molecular factors controlling ultrasonic therapy receptivity, however, are still not well understood. Because of the significant variability of the tumor microenvironment (TME), colorectal cancer (CRC) necessitates biomarker-guided techniques to enhance ultrasound-based therapy regimens. - Source: PubMed
Publication date: 2026/02/25
Zhang XiaohuiCao XuguangSu XinyaoHu WeiHou ShuoshuoZhou XiaohuaYang HongbaoJi Hongjian - Colon cancer is one of the most prevalent malignant tumors. Accurate evaluation of patient prognosis and optimization of treatment strategies continue to be major research focuses in colon cancer. Based on The Cancer Genome Atlas (TCGA) database, this study is the first to comprehensively analyze the expression, biological roles, and prognosis of itaconate and Hallmark pathway-related genes in colon cancer using bulk transcriptomics, single-cell transcriptomics, and spatial transcriptomics data. Through strict screening in 448 colon cancer patients from TCGA database (training set) and 7 colon cancer prognostic models from the Gene Expression Omnibus (GEO) database (including 1473 cases in the validation set), 10 prognosis-related genes (TIMP1, FJX1, CD36, CXCL1, ETS2, CDKN2A, INHBB, PLEC, TUBB2, and P4HA1) were selected. The optimal prognostic prediction model (Enet [alpha = 0.2]) was constructed and validated, which showed good prognostic predictive value in both the training and validation sets (average C-index > 0.7) and was superior to previous conventional clinical features and 22 prognostic models developed by researchers in the past 4 years. ScRNAseq (GSE225857) and spatial transcriptomics analyses clarified the cell-specific expression and spatial distribution characteristics of these genes in the tumor microenvironment (TME), with high functional scores mainly enriched in epithelial and stromal cells. Tissue microarray (TMA) showed that the high-risk group had higher tumor mutation burden (TMB) and higher expression of immune checkpoint genes, suggesting higher sensitivity to immunotherapy. Drug sensitivity analysis identified four potentially effective drugs, such as sepantronium bromide, which had better effects on high-risk patients. This study provides a theoretical basis and new targets for precise prognosis and stratified treatment of colon cancer. - Source: PubMed
Publication date: 2026/01/10
Zhang TingtingMeng JianchaoWang QingyunZhang PengLi HuiWei HailangChen DenggangBai ChenNair Sujit - Studies of the planar cell polarity (PCP) protein complexes Fat1/Fjx1 and Dchs/Fjx1 that form heterotypic interacting bridges of Fat1-Dchs between adjacent cells to confer PCP, as noted in Drosophila, are also found in mammalian cells and tissues as orthologs, such as in Sertoli cells and condensed spermatids in the seminiferous epithelium of the testis. Recent studies have shown that these two interacting PCP protein complexes are also crucial regulators of microtubule and actin dynamics, modulating the polymerization of both microtubules and actin filaments in the testis. In this review, we provide a brief update and thought-provoking concept on the PCP core proteins and the associated downstream signaling pathways utilized by PCP proteins to confer PCP and regulation of the microtubule and actin cytoskeletons in the testis. However, we focus on recent data in the field on the Fat1/Fjx1 and Dchs/Fjx1 protein complexes, which are also heterotypic interacting protein complexes, and their functional role in modulating the microtubule and actin cytoskeletal organization. Based on these recent findings, we formulate a hypothetic model depicting the role of these two PCP protein complexes in modulating the timely "opening" and "closing" of the blood-testis barrier (BTB) formed by adjacent Sertoli cells near the base of the seminiferous epithelium. Additionally, these two PCP protein complexes also modulate cytoskeletal dynamics between Sertoli cells and condensed spermatids to support haploid spermatid transport across the seminiferous epithelium during their structural transformation through spermiogenesis, and their eventual release at spermiation during the epithelial cycle of spermatogenesis. This hypothetical model will provide a useful framework for designing functional experiments to understand the role of PCP proteins in supporting spermatogenesis. - Source: PubMed
Bu TiaoWang LinglingWu XiaolongGao ShengYun DaminMao BaipingLi LinxiSun FeiCheng C Yan - Metformin, widely used for the treatment of type 2 diabetes, has recently gained attention for its potential anticancer properties. Several studies have shown that metformin treatment inhibits cell viability in colon adenocarcinoma (COAD); however, the research related to the tumor-node-metastasis (TNM) stage is limited. As COAD is frequently diagnosed at an advanced stage, understanding the genetic factors that regulate the pathogenesis of COAD at each TNM stage and the effects of metformin for potential treatment. Therefore, we identified differentially expressed factors at the TNM stage in metformin-treated COAD cells and investigated their regulatory mechanisms using microRNAs (miRNAs). Through bioinformatics analyses, four-jointed box kinase 1 (FJX1) and hsa-miR-1306-3p were identified as differentially expressed in COAD upon metformin treatment. Metformin treatment significantly reduced cell viability, with an observed decrease of approximately 50%. Analysis using quantitative real-time PCR showed an increase in hsa-miR-1306-3p and a decrease in FJX1 expression upon metformin treatment compared to untreated cells. Luciferase assay confirmed the sequence-specific binding of hsa-miR-1306-3p to FJX1. These findings highlight the potential of metformin as a therapeutic agent for COAD by modulating FJX1 expression via upregulation of hsa-miR-1306-3p, revealing novel avenues for COAD treatment. - Source: PubMed
Publication date: 2025/02/24
Kim Jung-MinShin Hae JinKim Woo RyungPark Eun GyungLee Du HyeongLee Yun JuJeong Hyeon-SuRoh Hyun-YoungKwon Ho JeongChoi Yung HyunLeem Sun-HeeKim Heui-Soo - Fat (FAT atypical cadherin) and Dchs (Dachsous cadherin-related protein) in adjacent Sertoli:Sertoli, Sertoli:spermatid, and spermatid:spermatid interfaces create an important intercellular bridge whose adhesive function is in turn supported by Fjx1, a nonreceptor Ser/Thr protein kinase. This concept is derived from earlier studies of Drosophila, which has been confirmed in this and earlier reports as well. Herein, we use the approach of knockdown of Fat1 by RNAi using primary cultures of Sertoli cells that mimicked the blood-testis barrier (BTB) in vivo, and a series of coherent experiments including functional assays to monitor the Sertoli cell tight junction (TJ) permeability barrier and a functional in vitro TJ integrity assay to assess the role of Fat1 in the testis. It was shown that planar cell polarity (PCP) protein Fat1 affected Sertoli cell function through its modulation of actin and microtubule cytoskeletal function, altering their polymerization activity through the Fat1/Fjx1 complex. Furthermore, Fat1 is intimately associated with β-catenin and α-N-catenin, as well as with Prickle 1 of the Vangl1/Prickle 1 complex, another PCP core protein to support intercellular interactions to confer PCP. In summary, these findings support the notion that the Fat:Dchs and the Vangl2:Fzd PCP intercellular bridges are tightly associated with basal ES/TJ structural proteins to stabilize PCP function at the Sertoli:Sertoli, Sertoli:spermatid, and spermatid:spermatid interface to sustain spermatogenesis. - Source: PubMed
Bu TiaoWang LinglingWu XiaolongGao ShengLi XinyaoYun DaminYang XiwenLi LinxiCheng Chuen YanSun Fei