Hence, a deeper investigation into the molecular mechanisms of SPOP in prostate cancer will provide novel insights into its physiological function in oncogenesis and drug development. In this review, we summarize SPOP's tumor suppressor functions and structural features, upstream regulatory mechanisms, and SPOP-targeting therapeutic strategies in prostate cancer.
Effect size estimates were relatively large for both the group effect (partial η2=0.20) and the time x group interaction (partial η2=0.24), suggesting that the study may have been underpowered to detect this difference statistically. In conclusion, the present exploratory study suggests that suramin exerts a dual antitumor effect on tongue squamous cell carcinoma by suppressing proliferative transcriptional programs, and modulating extracellular and stress response pathways, providing a basis for future studies to further elucidate its therapeutic relevance.
NDMA likely promotes BLCA through multi-target and multi-pathway mechanisms. The identified core genes serve as potential diagnostic biomarkers, and the proposed AOP provides a theoretical basis for environmental risk assessment and targeted intervention strategies.
In vitro, CCNB1 knockdown triggered cell cycle arrest, thereby suppressing the proliferation of colorectal cancer cells. This study validated CCNB1 as a dual-purpose biomarker for CRC diagnosis and favorable prognosis, highlighting its potential utility in clinical management.
We have established the correlation between the pathogenesis of GC's "cold and heat disorder" and modern pathological indicators (inflammation, oxidative damage, and cell apoptosis disorder) from the perspective of traditional Chinese medicine syndrome, providing a theoretical basis for the clinical application of BXXXD. The online version contains supplementary material available at 10.1007/s10616-025-00888-3.
2 months ago
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CDC20 (Cell Division Cycle 20) • CDK1 (Cyclin-dependent kinase 1) • KIF11 (Kinesin Family Member 11) • KIF20A (Kinesin Family Member 20A) • KIF2C (Kinesin Family Member 2C)
These agents exhibited superior anti-tumor efficacy compared with AR antagonists in vitro. Our study identified novel prostate cancer therapeutic targets independent of the AR signaling pathway and established a research paradigm for developing anti-tumor agents through integrative cancer bioinformatics and network pharmacology analysis.
Importantly, follow-up kinase selectivity profiling revealed that BDE30671203 is a highly selective PLK1 inhibitor, showing over 450-fold and 1200-fold selectivity against the closely related AURKA and AURKB kinases, respectively. Therefore, this study not only provides promising chemical starting points for PLK1-targeted drug discovery, but more significantly validates a robust screening strategy for kinase inhibitor discovery.
2 months ago
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BCL2 (B-cell CLL/lymphoma 2) • AURKA (Aurora kinase A) • PLK1 (Polo Like Kinase 1) • AURKB (Aurora Kinase B) • CDC20 (Cell Division Cycle 20) • CDK1 (Cyclin-dependent kinase 1)
The results emphasizes that EGCG has strong binding affinity towards YWHAZ, revealing that miR-30a-EGCG targets TNBC synergistically through cell-cycle-mediated pathways. The findings give rational support for miRNA-guided phytochemical-based TNBC therapeutic development.
The phosphorylation of key regulators involved in DNA repair and damage prevention, as well as MAPKs activated by C-ions irradiation, was partially inhibited by the combination treatment with crizotinib. While crizotinib shows promise as a therapeutic agent for sacral chordomas, its capacity to enhance radiosensitivity appears limited.
Overexpression of WDR77 also increased CDC20 protein levels. WDR77 serves as both a prognostic biomarker and functional regulator in melanoma, highlighting its potential as a therapeutic target.
A competing endogenous RNA (ceRNA) network involving miRNAs (e.g., miR-16-5p, miR-126-5p) and lncRNAs (e.g., AC008124.1, AC064799.2, AGAP11) potentially modulates their expression. This study identifies seven novel candidate biomarkers dysregulated in endothelial cells under combined BCR-ABL and exosomal stimulation, shedding light on the molecular crosstalk between leukemic cells and the vascular niche.