STMN1 (Phospho-Ser62) Antibody
- Known as:
- STMN1 (Phospho-Ser62) Antibody
- Catalog number:
- 11722
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- STMN1 (Phospho-Ser62) Antibody
Related genes to: STMN1 (Phospho-Ser62) Antibody
- Gene:
- STMN1 NIH gene
- Name:
- stathmin 1
- Previous symbol:
- LAP18, C1orf215
- Synonyms:
- SMN, OP18, PR22, PP19, PP17, Lag, FLJ32206
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1990-12-17
- Date modifiied:
- 2014-11-19
Related products to: STMN1 (Phospho-Ser62) Antibody
Related articles to: STMN1 (Phospho-Ser62) Antibody
- The tumor leading edge (TLE) is a critical region where tumor cells interact with the microenvironment to drive invasion and metastasis; however, its cellular architecture in early hepatocellular carcinoma (HCC) remains poorly understood. Here, we integrated single-nucleus RNA-seq (snRNA-seq), spatial transcriptomics, and computational pathology to investigate TLE in early HCC. We annotated 35 cell subpopulations and identified STMN1-high tumor cells as a key malignant subset enriched at the invasive front, interacting with Treg, plasma B, LAMP3⁺ dendritic cells and SPP1⁺ macrophages. Spatial analysis revealed three co-localized cell pairs-(SPP1⁺ macrophages co-localized with Tip-like and inflammatory endothelial cells), (LAMP3⁺ DCs co-localized with naive T cells), and (plasma B cells co-localized with cancer-associated fibroblasts)-forming a leading-edge tumor microenvironment (L-TME) niche associated with early relapse. We developed an L-TME-related machine-learning benchmark framework incorporating 71 imaging features (65 deep-learning + 6 pathological) based on the snRNA-seq, spatial transcriptomics and pathomics. The pathology model achieved robust performance (mean C-index=0.77) and successfully predicted the recurrence of early HCC (log-rank < 0.05) in TCGA (n=147) and an independent in-house cohort (n=123). This study delineates the TLE cellular ecosystem of early HCC, defines a spatially coordinated immunosuppressive L-TME niche, and provides a clinically applicable predictive tool for postoperative recurrence. Integrating multi-omics with computational pathology deepens our understanding of early HCC metastasis and offers insights into improved prognostication and therapeutic strategies. - Source: PubMed
Publication date: 2026/09/10
Wang XichengMu XiaolanFu YongDong WeiLu WenfengLi XiuhuaSong YanxiangLiu ChangchengHou BaojuZhang HaibinChen XiongCai YongchaoHe Zhiying - The tumor microenvironment (TME) of gastric adenocarcinoma is exceptionally heterogeneous, and epithelial-mesenchymal transition (EMT) is a central mechanism promoting local invasion and metastatic spread. Even so, how EMT-programmed cells are spatially arranged within tumor tissue, how they interact with neighboring immune populations, and which molecular nodes might be exploited therapeutically remain incompletely defined. - Source: PubMed
Publication date: 2026/09/07
Li JianwenQin ZitongWang TingLi WeipingMa JinminGuan Quanlin - Paclitaxel is a cornerstone microtubule-stabilizing agent, but intrinsic and acquired resistance limit durable benefit. Resistance emerges from interacting changes in drug transport, tubulin composition, microtubule regulation, mitotic fate, apoptosis, autophagy, cellular plasticity and the tumor microenvironment. The stathmin family-STMN1, STMN2, STMN3 and STMN4-controls microtubule assembly through tubulin sequestration and catastrophe-promoting activity and therefore occupies a direct functional interface with paclitaxel pharmacodynamics. STMN1 has the strongest evidence: overexpression can reduce taxane sensitivity, whereas suppression restores microtubule stabilization and drug response in several experimental systems; clinical studies also associate high STMN1 with unfavorable outcome or reduced taxane benefit in selected cancers. Evidence for STMN3 is narrower but includes a mechanistically relevant ovarian-cancer study in which bisphosphorylated PEA-15 sensitized cells to paclitaxel by attenuating SCLIP/STMN3-mediated microtubule destabilization. By contrast, direct evidence for STMN2 and STMN4 in taxane response remains insufficient. This review develops a microtubule-centered resistance model, distinguishes established findings from context-dependent observations and testable hypotheses, and evaluates biomarker and therapeutic strategies targeting stathmin expression, phosphorylation, stability and protein interactions. We propose that stathmin activity is most likely to have clinical value as part of a composite taxane-response classifier that also incorporates intracellular drug exposure, tubulin isotypes and apoptotic competence. - Source: PubMed
Publication date: 2026/09/01
Li HaoyuShi LizhouWang QinghuaHan Wei - Gastric cancer is a heterogeneous disease in which cancer stem cell-associated properties may contribute to tumor heterogeneity and progression. This study aimed to establish paired normal and tumor gastric organoids, characterize stemness-related gene expression, and explore its association with organoid formation. - Source: PubMed
Publication date: 2026/08/31
Yoo Yie-RiJeong KyoungyunYoo JaeunKim Hyun MyongShin Ji-YeonKang Min KyuPark KyoyoungKim Sa-HongKim ChungyoonKim JeesunPark Young SukKong Seong-HoLee Hyuk-JoonYang Han-KwangPark Do Joong - 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