Ask about this productRelated genes to: HOXC4 antibody
- Gene:
- HOXC4 NIH gene
- Name:
- homeobox C4
- Previous symbol:
- HOX3, HOX3E
- Synonyms:
- -
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-09-07
Related products to: HOXC4 antibody
Related articles to: HOXC4 antibody
- High-grade serous ovarian carcinoma is the most common and aggressive form of ovarian cancer, accounting for over 60% of cases and nearly 75% of deaths, mainly due to late diagnosis and tumor aggressiveness. Standard treatment is platinum-based chemotherapy with paclitaxel, but relapse is frequent. This study aimed to identify prognostic biomarkers for patients with poor survival outcomes after Taxol treatment using bioinformatics analysis. We examined the effects of mRNA expression and other markers on overall survival in serous ovarian cancer using the TCGA database, applying a multivariate Cox model that included interaction terms to identify -dependent and independent prognostic markers, and controlling for age and treatment type. Candidate -independent prognostic markers from TCGA were further validated using patient data from the KMplotter database. High mRNA expression emerged as a prognostic biomarker for three potential gene targets (, , and ) associated with improved OS at low levels of gene target expression, we identified four additional markers (, /, , and ) that exhibited a -independent negative correlation between mRNA expression and OS across the full spectrum of gene expression values in the ovarian cancer cohort validated using independent dataset from KMplotter, for Taxol-treated ovarian cancer patients. This study proposes a panel of potential prognostic biomarkers for the treatment of ovarian cancer patients, particularly by leveraging -dependent mRNA expression as a significant biomarker, alongside four additional -independent prognostic markers, for patients undergoing Taxol-based therapies. Future prospective clinical trials will be required to validate these prognostic markers. - Source: PubMed
Publication date: 2025/12/10
Qazi SanjiveRichardson StephenPotts MikeMyers ScottSaund SaranDe TapasTrieu Vuong - - Source: PubMed
Park Seok-RaeZan HongPal ZsuzsannaZhang JinsongAl-Qahtani AhmedPone Egest JXu ZhenmingMai ThachCasali Paolo - Fibrosis, characterized by excessive extracellular matrix (ECM) accumulation and fibroblast proliferation, significantly contributes to global morbidity and mortality, affecting millions worldwide. Despite its prevalence, the mechanisms underlying fibrotic skin diseases remain poorly understood, and effective treatments are scarce. This study leverages single-cell RNA sequencing (scRNA-seq) to unravel the heterogeneity of fibroblasts in fibrotic skin diseases, including normal skin, scar, keloid, and scleroderma. Through comprehensive analysis of scRNA-seq data from public repositories, we identified distinct fibroblast subpopulations specific to each fibrotic condition. Notably, pivotal regulators for each sub-fibroblast cluster were discovered: IRF4 for scar, CLOCK for keloid, RUNX3 for scleroderma, and HOXC4 for normal skin. Further, CLOCK was found to be predominantly expressed in keloid tissues, with its upregulation enhancing fibroblast proliferation and migration in vitro. Analysis of The Cancer Genome Atlas (TCGA) data revealed that CLOCK and its regulon genes were upregulated in skin cutaneous melanoma and even more so in metastatic tumors. Our findings underscore the utility of scRNA-seq in dissecting the cellular complexity of fibrotic skin diseases and highlight potential therapeutic targets. This study not only advances our understanding of fibroblast heterogeneity in fibrosis but also opens avenues for targeted therapeutic strategies, moving closer to personalized medicine for fibrotic diseases. - Source: PubMed
Publication date: 2025/12/06
Li YueLi ChangminLiu WeiGao TianbaoLiu QinYang LingLi SongtaoTang RuiYang Lei - Bone mineral density (BMD) is a key indicator of osteoporosis, which may influence the development of intervertebral disc degeneration (IDD). However, the causal relationship and underlying signaling pathways between BMD and IDD remain unclear. Therefore, this study aimed to investigate the potential causal relationship and underlying signaling pathways between BMD and IDD. A two-sample Mendelian randomization (MR) analysis was employed to analyze the causal effects of BMD levels across 3 anatomical sites [total body BMD (TB-BMD), lumbar spine BMD (LS-BMD), and femoral neck BMD (FN-BMD)] on risks of IDD. In this study, IDD was divided into 2 groups, namely cervical IDD (C-IDD) and thoracic/thoracolumbar/lumbosacral IDD (TTL-IDD). Additionally, multivariable MR (MVMR) was applied to explore whether type 2 diabetes (T2D) and body mass index (BMI) would mediate the identification of causal pathways. Moreover, gene ontology (GO) enrichment analysis and expression quantitative trait locus (eQTL) colocalization analyses were utilized to examine the potential mechanisms and shared genes involved in osteoporosis and IDD. The results showed that genetic predispositions to TB-BMD, LS-BMD, and FN-BMD were associated with increased risk of C-IDD. Furthermore, TB-BMD, LS-BMD, and FN-BMD were identified as significant risk factors causally associated with TTL-IDD. The MVMR analysis revealed that even after adjusting for T2D and BMI, lower TB-BMD could significantly increase the odds of C-IDD and TTL-IDD. In the subgroup analysis, a significant causal effect of TB-BMD on TTL-IDD was observed in individuals aged 30 to 45, 45 to 60, and > 60 years. Polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3) and homeobox C4 (HOXC4) were the most prominent co-located genes illustrated by GO enrichment analysis and eQTL analysis. In conclusion, we found that lower BMD exerts significant causal effects on elevated IDD risk (both C-IDD and TTL-IDD). - Source: PubMed
Huang LongaoYang QinghuaXu HongyuanFeng JunfeiLiu DunJiang Hua - Organisms living in desert habitats face multiple simultaneous pressures, such as high temperatures and arid, and the population dynamics and community diversity of small rodents are strongly affected by climate extremes. However, the potential mechanisms by which desert rodents adapt to arid remain largely unexplored. Here, we assembled a 3.18 Gb genome, including 25,812 protein-encoding genes, for Orientallactaga sibirica, which is widely distributed across both arid and semihumid environments in Eurasia. Orientallactaga sibirica has longer ears and hind limbs to enhance heat dissipation, which may be related to the positively selected genes, such as Fgf10, Fgf11, Hoxc4, Hoxd1, and Bmp4. The renal transcriptome revealed increased fat and carbohydrate metabolism for metabolic water production in O. sibirica residing in arid habitats. Pathways such as material metabolism, oxidative stress response, osmoregulation, and water and salt reabsorption were enriched in candidate genes, such as Avp, Ang, and Ace, under positive selection in O. sibirica. Moreover, amino acid replacement was observed in the protein sequences of seven candidate genes, including Aldh7a1, Lnpep, Wnk4, C1qc, and Awat2, and these specific amino acid replacements of genes such as Umod and Scnn1a were related to unique osmoregulation, osmotic protection, and water retention compensation mechanisms. Water deprivation under laboratory conditions induced the upregulation of Umod and Aldh7a1 expression, further supporting the results observed in the wild population. These findings demonstrate that the positively selected genes related to limb development and specific amino acid replacements in the genes Umod and Scnn1a for unique osmoregulation in the renal vascular system may contribute to arid adaptation in the desert rodent species O. sibirica. This study provides novel insights into the adaptive evolution of desert small mammals and can serve as a reference for future research on renal damage-related diseases, such as human kidney stones and salt-sensitive hypertension. - Source: PubMed
Yuan ShuaiZhang RongJin YonglingLi XinLi LinlinZhang DongLing YuZhang KaijianWu XiaodongZhang XueyingFu Heping