^
Contact us  to learn more about
our Premium Content:  News alerts, weekly reports and conference planners
GENE:

CXXC5 (CXXC Finger Protein 5)

i
Other names: CXXC5, CXXC Finger Protein 5, Retinoid-Inducible Nuclear Factor, RINF, Putative NF-Kappa-B-Activating Protein 102, Putative MAPK-Activating Protein PM08, WT1-Induced Inhibitor Of Dishevelled, CXXC-Type Zinc Finger Protein 5, HSPC195, CF5, WID, CXXC Finger 5 Protein
14d
CXXC5 drove inflammation and ovarian cancer proliferation via transcriptional activation of ZNF143 and EGR1. (PubMed, Cell Signal)
Through in vitro and in vivo experiments, we confirmed ZNF143 and EGR1 as downstream transcription factors of CXXC5, mediating its proliferative potential in ovarian cancer. Our findings suggest that the CXXC5-ZNF143/EGR1 axis forms a network driving ovarian cell proliferation and tumorigenesis, and highlight CXXC5 as a potential therapeutic target for ovarian cancer treatment.
Journal
|
HIF1A (Hypoxia inducible factor 1, alpha subunit) • CXXC5 (CXXC Finger Protein 5) • EGR1 (Early Growth Response 1) • ZNF143 (Zinc Finger Protein 143)
|
HIF1A expression
3ms
Identification and validation of hub genes and molecular classifications associated with chronic myeloid leukemia. (PubMed, Front Immunol)
Finally, our clinical samples validated the expression and diagnostic efficacy of hub genes, and the knockdown of LINC01268 inhibited the proliferation of CML cells, and promoted apoptosis. Through WGCNA analysis and LASSO regression analysis, our study provides a new target for CML diagnosis and treatment, and provides a basis for further CML research.
Journal
|
CD8 (cluster of differentiation 8) • CXXC5 (CXXC Finger Protein 5)
6ms
Multi-omics analysis reveals critical metabolic regulators in bladder cancer. (PubMed, Int Urol Nephrol)
This study provides a comprehensive and systematic analysis, focusing on identifying key regulatory factors that may lead to cancer metabolic heterogeneity. Further understanding and verification of the cancer genes driving metabolic reprogramming and their role in the progression of bladder cancer will help to identify new therapeutic targets.
Journal
|
KDM6A (Lysine Demethylase 6A) • CXXC5 (CXXC Finger Protein 5)
10ms
Undifferentially Expressed CXXC5 as a Transcriptionally Regulatory Biomarker of Breast Cancer. (PubMed, Adv Biol (Weinh))
The overlapping long noncoding RNAs (lncRNAs) may have contributed their transcripts to the expression miscalculations of dark biomarkers. The mqTrans analysis serves as a complementary view of the transcriptome-based detections of biomarkers that are ignored by many existing studies.
Journal
|
CXXC5 (CXXC Finger Protein 5)
over1year
Zinc-finger Protein CXXC5 Promotes Breast Carcinogenesis by Regulating the TSC1/mTOR Signaling Pathway. (PubMed, J Biol Chem)
Meanwhile, a high expression of CXXC5 was positively correlated with the histological grade of high malignancy and poor survival of patients. In conclusion, our study revealed that CXXC5-mediated TSC1 suppression activates the mTOR pathway, reduces autophagic cell death, induces PD-L1-mediated immune suppression, and results in tumor development, shedding light on the mechanism of the pathophysiological function of CXXC5.
Journal • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • TSC1 (TSC complex subunit 1) • CXXC5 (CXXC Finger Protein 5) • CUL4B (Cullin 4B)
over1year
Context-dependent tumor-suppressive BMP signaling in diffuse intrinsic pontine glioma regulates stemness through epigenetic regulation of CXXC5. (PubMed, Nat Cancer)
Beyond showing how BMP signaling impacts DIPG, our study also identified the potent antitumor efficacy of Dacinostat for DIPG. Thus, our study delineates context-dependent features of the BMP signaling pathway in a DIPG subtype.
Journal
|
ACVR1 (Activin A Receptor Type 1) • CXXC5 (CXXC Finger Protein 5)
|
H3.3K27M • ACVR1 mutation
2years
Molecular and clinical characterization of the new WHO entity ‘Astroblastoma, MN1 altered’ and its molecular subgroups (AACR 2022)
The smaller subset of CXXC5-fused patients (n=8) indicated a 5/10 year OS of 83% and a 5/10 year PFS of 60% each. First analyses of BEND2-fused cases indicate that an Astroblastoma histology might be associated with a favorable OS, however further analyses, including a central pathology review, are needed to validate this observation.
Clinical
|
CXXC5 (CXXC Finger Protein 5)
over2years
Utilising artificial intelligence (AI) for analysing multiplex genomic and magnetic resonance imaging (MRI) data to develop multimodality predictive system for personalised neoadjuvant treatment of breast cancer (BC) (SABCS 2021)
Our predictive models were trained in a local cohort of 400 BC (300 HER2 negative (HER2-) received 8 cycles of anthracycline & Taxane & 100 HER2 positive (HER2+) received Trastuzumab, anthracycline &Taxane) & was validated in 150 patients from local clinical trial patients... A predictive model was developed for HER2+ and another for HER2- BC with >= 80% accuracy prediction of pCR. AI & multiplex technology could enable robust biomarker discovery.
Clinical
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • PGR (Progesterone receptor) • CCND1 (Cyclin D1) • TACC3 (Transforming acidic coiled-coil containing protein 3) • RAD51 (RAD51 Homolog A) • PIK3CD (Phosphatidylinositol-4 5-Bisphosphate 3-Kinase Catalytic Subunit Delta) • CDK6 (Cyclin-dependent kinase 6) • AGR2 (Anterior gradient 2) • GRB7 (Growth Factor Receptor Bound Protein 7) • CXXC5 (CXXC Finger Protein 5) • FOXM1 (Forkhead Box M1) • PMAIP1 (Phorbol-12-Myristate-13-Acetate-Induced Protein 1) • BAG1 (BAG Cochaperone 1) • FOXC1 (Forkhead Box C1) • SFRP1 (Secreted frizzled related protein 1) • TP73 (Tumor Protein P73) • MCM3 (Minichromosome maintenance complex component 3)
|
HER-2 positive • HER-2 overexpression • HER-2 negative • HER-2 expression • CCND1-H
|
Prosigna™ Breast Cancer Prognostic Gene Signature Assay • MammaPrint • Oncotype DX Breast Recurrence Score®Test
|
Herceptin (trastuzumab)
3years
[VIRTUAL] Understanding the biologic determinants of ribociclib efficacy in breast cancer (ESMO-BC 2021)
 In BC PDXs, B-L biology associates with lower response to ribociclib monotherapy than Luminal or HER2-E. Ribociclib induces a luminal phenotype with high GE of estrogen-regulated genes and low GE of proliferation genes, a biological switch that could explain the better efficacy of ribociclib in the endocrine therapy (ET)-resistant HER2-E subtype observed in clinical trials when combined with ET.
Clinical
|
HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • FOXA1 (Forkhead Box A1) • GRB7 (Growth Factor Receptor Bound Protein 7) • KRT17 (Keratin 17) • CXXC5 (CXXC Finger Protein 5) • KRT14 (Keratin 14) • CDH3 (Cadherin 3) • GPR160 (G Protein-Coupled Receptor 160) • KRT5 (Keratin 5) • MLPH (Melanophilin) • SFRP1 (Secreted frizzled related protein 1)
|
HR positive • HER-2 negative • HER-2 expression • MYC expression • HR positive + HER-2 negative
|
Prosigna™ Breast Cancer Prognostic Gene Signature Assay
|
Kisqali (ribociclib)