CCND1 (Cyclin D1)

Virtual screening and molecular dynamics simulations identified acetyldigitoxin (ADT) as a potent EZH2 inhibitor, demonstrating superior binding affinity (-10.90 kcal/mol) and complex stability compared to the known inhibitor GSK126...ADT induced G0/G1 cell cycle arrest and promoted apoptosis, accompanied by upregulation of pro-apoptotic genes (Bax, Caspase-3) and downregulation of anti-apoptotic (Bcl-2) and cell cycle (CyclinD1) genes. Our integrated findings position ADT as a repurposed drug candidate for targeting EZH2 in NSCLC, warranting further preclinical investigation including direct enzyme inhibition assays.

Structure-activity analyses identify flavanone glycosides and triterpenoids as promising scaffolds for medicinal chemistry optimization. Challenges, including poor bioavailability and off-target effects, necessitate advanced delivery systems and computational modeling to enhance selectivity and therapeutic utility, positioning these phytochemicals as viable leads for bone-related disorder treatments.

The present study suggests that SPINK1 may modulate glycolytic metabolism in lung cancer cells, inhibiting their growth and proliferation, and potentially providing therapeutic insights.

AAS exerts anti-ovarian cancer effects by impeding β-catenin nuclear translocation through inhibition of the Wnt pathway, resulting in coordinated downregulation of oncogenic effectors and dual suppression of proliferation and metastasis. Furthermore, this mechanism effectively induces apoptosis and cell cycle arrest in SKOV3 cells, highlighting its multifaceted antitumor potential.

The study identifies PDCD4 as a key therapeutic target and demonstrates that the PTX-TP@PLGA-iRGD nanocomplex enhances drug potency, selectivity and molecular engagement. This study offers a promising strategy to overcome metastasis and chemoresistance in colon cancer.

MYH9 acts as an oncogenic gene in SCC, which promotes the carcinogenesis and progression of SCC cells via EMT signaling, and it may serve as a valuable patent for targeted treatment biomarker of SCC.

The authors further evaluate the potential of SOX1 as a biomarker and therapeutic target in cancer diagnosis, treatment, prognosis, and associated complications. Although the functional heterogeneity of SOX1 presents challenges for clinical application, therapeutic modulation of its upstream and downstream pathways, as well as methylation-based assays for early detection, remain clinically promising.

We demonstrate that our model can predict a spheroid's long-term invasive fate with high accuracy using only partial image sets from early time-points, rather than the complete time-course images. Our work presents an in vivo -like, scalable 3D platform integrated with a quantitative high-throughput pipeline to elucidate GBM invasion mechanisms and to evaluate anti-invasive compounds.

A conservative re-excision was performed, and a PET/CT scan showed no evidence of dissemination. With 16 months of follow-up available, longer-term monitoring will be required to determine the clinical behavior and biologic potential of this tumor.

Moreover, Gossypol exhibited cytotoxic effects on human breast, prostate, and colorectal cancer cell lines, at least partially through downregulating the oncogenic substrates of targeted DUBs such as c-Myc, Mcl-1, MDM2, and Cyclin D1. Collectively, our findings position Gossypol as a promising small-molecule inhibitor targeting DUBs, especially USPs, and provide a rationale for further exploring its therapeutic potential in USP-driven cancers.

This study comprehensively explores the multi-target mechanisms of TKM against TNBC using network pharmacology, molecular pharmacology, and metabolomics approaches. These findings provide a foundation for future mechanistic investigations and may support the further preclinical development of TKM-based strategies for TNBC.

Silencing of SNHG10 decreases cell survival, proliferation, clonogenicity, EMT tumor growth through the EGFR/AKT/ERK/mTOR axis, and restores the expression of miR-150-5p, which eventually downregulates VEGF-A. SNHG10 downregulation enhanced the gemcitabine sensitivity in gemcitabine-resistant PDAC cells.