Ask about this productRelated genes to: TPX2 antibody
- Gene:
- TPX2 NIH gene
- Name:
- TPX2 microtubule nucleation factor
- Previous symbol:
- C20orf2, C20orf1
- Synonyms:
- p100, DIL-2
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-29
- Date modifiied:
- 2019-01-21
Related products to: TPX2 antibody
Related articles to: TPX2 antibody
- The hyperproliferation and aberrant inflammatory activation of epidermal keratinocytes constitute the core pathological features of psoriasis. While non-coding RNAs have emerged as critical epigenetic regulators, their specific contributions to psoriatic pathogenesis remain incompletely understood. In this study, we investigated the pathological significance of a novel circular RNA, circLDLR, which was identified via high-throughput sequencing and validated to be significantly upregulated in clinical psoriatic lesional tissues compared to normal skin. In vitro, utilizing an M5 cytokine-induced HaCaT keratinocyte model to mimic the psoriatic inflammatory microenvironment, we observed a concordant upregulation of circLDLR. Functional evaluations revealed that the targeted knockdown of circLDLR effectively mitigated M5-induced cellular hyperproliferation, pathological migration, and the excessive secretion of pro-inflammatory cytokines (IL-6, IL-1β, and IL-8). Mechanistically, RNA immunoprecipitation and dual-luciferase reporter assays elucidated that cytoplasmic circLDLR functions as a competing endogenous RNA (ceRNA) by physically sponging miR-1294, thereby de-repressing the expression of its downstream target, TPX2. Crucially, the phenotypic protection conferred by circLDLR silencing was significantly reversed by either miR-1294 inhibition or TPX2 overexpression. Collectively, our findings identify the circLDLR/miR-1294/TPX2 axis as a novel molecular driver of keratinocyte dysfunction, providing valuable histopathological insights and highlighting a promising therapeutic target for psoriasis. - Source: PubMed
Publication date: 2026/08/10
Tian JiangtianDeng XuanqiYin AnqiLiu WeiGao YugeLi YuzhenHao Siyu - - Source: PubMed
Publication date: 2026/08/10
Gu XiaoYao XiaocuiLiu Dengtao - : Colorectal cancer (CRC) remains a heterogeneous disease, and improved biomarkers are needed to support prognostic assessment. This study aimed to characterize hub genes in CRC and evaluate whether a gene signature provides biologically meaningful and prognostic information in clinical-genomic models. : We integrated three GEO microarray datasets (GSE110223, GSE110224, and GSE23878) to identify common differentially expressed genes using adjusted p<0.05 and ∣log2FC∣>1. Hub genes and protein expression were identified through protein-protein interaction network analysis using maximal clique centrality and Human Protein Atlas, respectively. Prognostic relevance was evaluated in TCGA-COAD/READ using Kaplan-Meier analysis, multivariable Cox regression, Cox-derived prognostic indices, time-dependent ROC analysis, and regression-based machine learning for internal robustness. Principal component analysis (PCA) was used to derive a standardized PC1-based score from the 10-hub gene signature. : A ten-gene mitotic hub signature (TPX2, UBE2C, AURKA, NEK2, PRC1, CCNB1, CDK1, CEP55, FOXM1, and RRM2) was consistently upregulated across the three datasets and enriched for cell-cycle and mitotic pathways. Protein-level and survival analyses supported the biological relevance of several hub genes. In TCGA-COAD/READ, the signature showed limited standalone prognostic value and did not retain independent significance after adjustment for clinical variables, although it contributed modestly in integrated clinical-genomic models. PCA showed a one-dimensional signature, with PC1 capturing the dominant shared expression pattern. Gradient Boosting Regressor (R = 0.8035, MSE = 0.0473) supported the internal robustness of the DEG-based expression pattern. : The ten-gene mitotic hub signature represents a coherent CRC-related proliferative program with limited value as an isolated prognostic marker, but it may still be useful as part of integrated risk models that require external validation. - Source: PubMed
Publication date: 2026/07/08
Kamal EbtihalMoglad EhssanMohager Samah OAhmed MehadAldoseri Mobarak MahfodSuwayyid Barakat A AlBawadood Azizah SalimHamdan Hamdan ZAkbulut Mikail - Esophageal squamous cell carcinoma (ESCC) faces challenges of metastasis and variable radiosensitivity. The role of Targeting Protein for Xenopus Kinesin-like Protein 2 (TPX2) in regulating these ESCC-related traits is unclear, needing investigation. - Source: PubMed
Publication date: 2026/07/01
Meng FangHu JiaruZhang ShiqiangShi QifengChang NaZhu Yaqun - Chromosomal instability (CIN) arising from mitotic errors is a hallmark of cancer progression, yet how specific spindle assembly factors are co-opted to support aggressive tumor phenotypes remains incompletely understood. Hepatoma Upregulated Protein (HURP/DLGAP5), a Ran-regulated microtubule-associated protein essential for kinetochore fiber stabilization and chromosome congression, is frequently overexpressed in aggressive cancers. Here, we investigated HURP's role across a breast cancer metastatic gradient-immortalized MCF10A, the low-metastatic luminal T47D, and the highly metastatic triple-negative MDA-MB-231 cell lines-integrating quantitative spindle analysis, kinetochore tension measurements, spindle checkpoint profiling, migration dynamics, and three-dimensional spheroid modeling. We show that total HURP protein levels increase with metastatic potential, yet spindle-bound HURP is paradoxically reduced in MDA-MB-231 cells, indicating cytoplasmic mislocalization despite increased total protein levels. HURP silencing induced cell-line-specific defects: moderate disorganization and misorientation in MCF10A and T47D cells, but catastrophic spindle collapse, apoptosis, and G2/M arrest in MDA-MB-231 cells. Mechanistically, HURP depletion disrupted the spindle-associated levels and distributions of TPX2, Aurora-A, and NuMA in a subtype-dependent manner, implicating HURP as a context-dependent stabilizer of this mitotic regulatory axis. HURP loss reduced interkinetochore tension in all cell lines, but only MCF10A and T47D cells mounted a proportional BubR1-dependent checkpoint response; MDA-MB-231 cells showed reduced checkpoint signaling, consistent with constitutive spindle assembly checkpoint (SAC) attenuation in triple-negative breast cancer. Beyond mitosis, HURP depletion impaired collective migration and converted MDA-MB-231 cells from super-diffusive, amoeboid-like motility to sub-diffusive behavior, while minimally affecting the less aggressive cell lines. HURP-depleted MDA-MB-231 spheroids were significantly larger, less compact, and less spherical than controls, linking spindle regulation to tissue-level architectural coherence. These findings establish HURP as a multifunctional regulator coordinating mitotic fidelity, migration plasticity, and tumor architecture in breast cancer, with a selective dependency in highly metastatic cells, positioning it as a promising therapeutic target for aggressive breast cancers. - Source: PubMed
Publication date: 2026/06/30
Efstathiou ChristosDidaskalou StylianosKarkaletsou LitoMalichetoudi StellaEftalitsidis EvgeniosGirod AndreasKoffa Maria