SCREW CAP, DEEP, RED,500_BAG
- Known as:
- SCREW CAP, DEEP, RED,500_BAG
- Catalog number:
- T666-R
- Product Quantity:
- 1PK
- Category:
- -
- Supplier:
- BioBasic
- Gene target:
- SCREW CAP DEEP RED 500_BAG
Related genes to: SCREW CAP, DEEP, RED,500_BAG
- Gene:
- SPAG5 NIH gene
- Name:
- sperm associated antigen 5
- Previous symbol:
- -
- Synonyms:
- DEEPEST, MAP126, hMAP126
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-08
- Date modifiied:
- 2008-07-18
Related products to: SCREW CAP, DEEP, RED,500_BAG
Related articles to: SCREW CAP, DEEP, RED,500_BAG
- Glioblastoma (GBM) is among the most aggressive primary brain tumors, marked by rapid proliferation, therapeutic resistance, and profound intratumoral heterogeneity. Epigenetic regulators such as lysine-specific demethylase 1A (KDM1A) and histone deacetylase 2 (HDAC2) are aberrantly expressed in resistant GBM subpopulations and strongly correlate with poor clinical outcomes. Here, we assessed the therapeutic potential of MPT0G521, a dual KDM1A/class I HDAC inhibitor, in disrupting epigenetic regulation and cell cycle progression. Bioinformatic analyses of resistance-associated gene profiles (temozolomide and 2 Gy radiation) and single-cell transcriptomic datasets from distinct tumor regions revealed enrichment of KDM1A and HDAC2 in high-cycling GBM clusters, particularly at invasive margins prone to recurrence. Functional assays demonstrated that MPT0G521 potently inhibited proliferation of both parental and temozolomide-resistant GBM cells, inducing G2/M arrest and apoptosis. Transcriptomic profiling further identified significant downregulation of centrosome integrity genes (FSD1, KIFC1), spindle regulators (TUBB, STMN1, KIF2C, KIF15), kinetochore components (AURKB, CDCA8, SPAG5), and G2/M checkpoint mediators (CENPF, MYBL2, CCNF, MYT1, CDC25A), resulting in disrupted mitotic progression. Mechanistically, MPT0G521 increased histone H3 methylation and acetylation, validating its dual inhibitory activity against KDM1A and class I HDACs. Collectively, these findings indicate that MPT0G521 disrupts the G2/M activation and mitotic machinery, thereby suppressing proliferative and resistant GBM subpopulations. This dual epigenetic strategy holds strong promise for overcoming GBM heterogeneity and reducing recurrence. - Source: PubMed
Publication date: 2026/09/02
Wu An-ChihChuang Jian-YingLiu Jr-JiunSalim Enrica AngelinaWu Ming-HsiaoJing Shih-WeiHsu Tsung-IChang Kwang-YuChang Wen-ChangThakur AmandeepLiou Jing-PingLo Wei-Lun - - Source: PubMed
Publication date: 2026/05/28
Ma MinWu HaixiaoZhu DeshengSun PengJiang JiaweiWang LeiYang QingXu Min - Colorectal cancer (CRC) has a high incidence and mortality rate worldwide, with chemotherapy being a cornerstone of treatment for locally advanced CRC patients (LACRC). Despite the relatively high efficacy of chemotherapy regimens like FOLFOX and CAPEOX, the resistance of chemotherapy remains a significant challenge. In this study, we identified sperm associated antigen 5 (SPAG5) as a potential therapeutic target in LACRC patients. High SPAG5 expression was correlated with improved progression-free survival (PFS) and overall survival (OS) in CRC patients receiving chemotherapy, as demonstrated by analyses of multiple cohorts, including TCGA, GEO and FUSCC. Mechanistically, SPAG5 overexpression promoted ferroptosis in CRC cells, enhancing chemotherapy efficacy through increased reactive oxygen species (ROS). SPAG5 depletion reduced ROS levels, attenuated ferroptosis, and decreased the cytotoxic effects of chemotherapy. These results indicate that SPAG5 can modulate ROS-dependent ferroptosis to enhance the chemotherapeutic response. Furthermore, inhibition of ROS reversed the chemotherapy-sensitizing effect mediated by SPAG5. Together, these findings suggest that SPAG5 may serve as a promising biomarker and therapeutic target to potentiate the cytotoxic effects of chemotherapy in LACRC patients. - Source: PubMed
Publication date: 2026/03/03
Gu RuiqiFang HongshengXu YunpuWang HoumingCai GuoxiangZheng JiujianWang RenjieDai Weixing - PURPOSE: Malignant mesothelioma is a rare, aggressive cancer. Although the World Health Organization (WHO) histologic subtypes–epithelioid (best prognosis), biphasic, and sarcomatoid (worst prognosis)—provide baseline stratification, architectural and molecular features (e.g., aneuploidy, immune infiltration) introduce heterogeneity not fully captured by histotype alone. METHODS: Using The Cancer Genome Atlas (TCGA) data and an independent validation cohort, we found that TNM stage was not independently prognostic after multivariable adjustment. We therefore developed a clinicomolecular model integrating transcriptomic and clinicopathological variables. Differential expression analysis of TCGA tumors identified 1,055 genes associated with poor prognosis (FDR < 0.05, |log2FC| > 1). Least absolute shrinkage and selection operator (LASSO) followed by multivariate Cox regression yielded five independent predictors: pathological subtype, receipt of pharmaceutical (systemic) therapy, and tumor expression of SPAG5, CORO1C, and SGCE. The final score was: RiskScore = 1.590 × (pathological type) − 2.258 × (pharmaceutical therapy) + 3.048 × SPAG5 + 1.652 × CORO1C + 0.908 × SGCE. RESULTS: In the TCGA cohort, high-risk patients had significantly shorter overall survival (log-rank p < 0.001), and time-dependent ROC AUCs exceeded 0.70 at 1–5 years. In the validation cohort, the RiskScore significantly stratified overall survival (log-rank p < 0.001) and demonstrated superior predictive accuracy over both TNM staging and the established European Organization for Research and Treatment of Cancer (EORTC) prognostic score. CONCLUSION: This clinicomolecular model provides prognostic discrimination superior to TNM stage and EORTC score, offering a robust tool for risk-stratified management of mesothelioma. - Source: PubMed
Publication date: 2026/02/08
An QingzhengCui FengyunShi GuangmingNi LongkunXiao KunTian FengChen YuezhiLi LepingJing ChangqingLian Guodong - To date, immune checkpoint inhibitors (ICIs) have emerged as a leading treatment for metastatic cancer, significantly improving patient survival while causing relatively few side effects. However, the objective response rate for ICIs remains low approximately 30% in urothelial carcinoma (UC), underscoring the urgent need for predictive response biomarkers. Several state-of-the-art signatures have been revealed in top-tier journals, highlighting the importance of this field. As the number of genes (~20,000) far exceeds the sample sizes of typical training sets (generally ≤ 300), we first developed feature selection procedures to reduce the number of features to a few hundred. We then trained multiple machine learning classifiers using the selected genes and the IMvigor210 dataset, which includes RNA-seq and clinical data from ~298 patients with metastatic UC (mUC). Notably, our predictor LogitDA, using the identified 49-gene signature, achieved a prediction AUC of 0.75 in an independent dataset, PCD4989g(mUC). Moreover, our signature outperformed six state-of-the-art signatures, PD-L1 IHC, and five tumor microenvironment signatures, including IFN-γ, T-effector, and T-cell exhaustion signatures. When we integrated each of the six known signatures with our own, our signature still surpassed the integrated ones in terms of prediction AUC and accuracy in the PCD4989g(mUC) dataset. From our signature, we identified key prognostic biomarkers, with the top five markers LYRM1, RFC4, CENPL, SPAG5, and CACYBP (Benjamini-Hochberg adjusted P < 0.0025) in the IMvigor210 dataset. Finally, we performed pathway analyses using Reactome (MSigDB) and KEGG, to reveal some immune-related pathways enriched such as MHC class II antigen presentation. - Source: PubMed
Publication date: 2025/11/20
Langfelder PeterLin En-TniTsai Yi-TaCha Tai-LungShieh Grace S