Mouse polyclonal to UNC5D, Host Mouse
- Known as:
- Mouse pab UNC5D, Host Mouse
- Catalog number:
- YF-PA26889
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal UNC5D Host
Ask about this productRelated genes to: Mouse polyclonal to UNC5D, Host Mouse
- Gene:
- UNC5D NIH gene
- Name:
- unc-5 netrin receptor D
- Previous symbol:
- -
- Synonyms:
- KIAA1777, Unc5h4
- Chromosome:
- 8p12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-13
- Date modifiied:
- 2016-12-16
Related products to: Mouse polyclonal to UNC5D, Host Mouse
Related articles to: Mouse polyclonal to UNC5D, Host Mouse
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Rao HuiXie GuanboWu NingLi JinHan Xiao - Metastasis remains the primary cause of breast cancer mortality. Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype. It lacks targeted therapies and carries a high risk of metastasis. MiRNAs are one of the potential diagnostics and therapeutic biomarkers, given that the regulation of mRNA is critical for tumor growth and metastatic transformation of tumor cells. Identifying the differential expression of the miRNA-mRNA axis at the primary tumor site will provide novel molecular mechanisms for metastasis initiation. In this study, we applied an integrated approach to explore the metastasis-specific miRNA-mRNA regulatory axis in TNBC using TCGA-derived miRNA-seq and RNA-seq data. Differential expression analysis between metastatic and non-metastatic TNBC patient data identified 11 dysregulated miRNAs, of which 8 showed linear expression changes with increasing disease aggressiveness. Among them, hsa-miR-1-1/2, hsa-miR-9, and hsa-miR-1180 displayed strong diagnostic potential (AUC >0.8) and significant associations with overall survival in metastatic TNBC patients. Parallel RNA-seq analysis revealed 36 differentially expressed genes (DEGs). Target prediction highlighted that only hsa-miR-9-5p targeted three of the 36 DEGs-FABP7, GPR26, and UNC5D, where FABP7 demonstrated strong association with cancer pathways. The expression of these genes was also correlated with the overall survival of the TNBC patients. Validation of this axis in various breast cancer cells (metastatic and non-metastatic) was performed, and the results indicated an inverse expression pattern of hsa-miR-9-5p and FABP7, especially in metastatic TNBC cells. These findings propose the hsa-miR-9-FABP7 axis as a promising biomarker signature for predicting metastatic potential from primary TNBC tumors. - Source: PubMed
Publication date: 2026/07/24
Rathore DeepshikhaDheer VasundharaSingh SurbhiPatel ShanayaDesai ChiragDave Heena V - Oral Submucous Fibrosis (OSMF) is a significant global oral health problem, particularly prevalent in India, with a high risk of progression to Oral Squamous Cell Carcinoma (OSCC). This study investigates the molecular mechanisms involved in the transformation of OSMF to OSCC using transcriptomic profiling. High-throughput RNA sequencing was performed on fresh de novo OSCC samples ( = 8) and OSMF derived OSCC using Illumina-compatible NEXTflex Rapid Directional RNA Sequencing. Normalization and differential gene expression analysis were conducted, and genes exhibiting an absolute log2 fold change of ≥2 with a co-variate-adjusted -value ≤ 0.05 were identified as significant. Upregulated genes were associated with cytokine and immune responses (ABRA, TTTY14, EIF1AY), cellular proliferation and apoptosis (LINC00314, RPS4Y1, SERPINA5, TRIM63, FABP7), and energy metabolism, indicating metabolic adaptations during malignant progression. Pathway analysis showed increased expression of TNNT1, TNNI1, MYL4, and ACTN3, implicating muscle development and embryonic pathways in OSMF transformation. Conversely, genes related to epithelial differentiation and keratinization (FLG, FLG2, HRNR, TCHH, KRT73), immune regulation and tumor suppression (HLA-G, UNC5D), and metabolic signaling were downregulated, reflecting loss of tissue integrity and immune control. OSMF-derived OSCC exhibits a distinct transcriptomic landscape compared with de novo OSCC, characterized by altered epithelial differentiation, immune modulation, and activation of developmental pathways. The observed gene dysregulation findings establish that OSCC developing in the background of OSMF is molecularly distinct from de novo OSCC, underscoring the biological impact of the pre-existing fibrotic milieu on tumor transcriptional architecture. - Source: PubMed
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