CASP7 (Caspase 7)

Viability, cytotoxicity, and caspase-3/7 activity were assessed following single-agent treatment with asciminib, ponatinib, bortezomib, or panobinostat. Co-inhibition of proteasomes and histone deacetylases eliminates TKI-refractory BCR::ABL1-driven leukaemia cells by inducing mitochondrial apoptosis and loss of clonogenic potential. These findings indicate a clinically actionable, TKI-independent strategy for the salvage treatment of multidrug-resistant CML.

These results question the conventional in vitro focus on cardiomyocytes regarding drug-induced cardiac damage, highlighting the interplay among different cardiac cell types in mediating the toxic effects of doxorubicin. Furthermore, the work demonstrates the potential of AI-based tools to provide scalable strategies for assessing drug-induced cardiotoxicity.

Significant proportions of fragmented DNA (25.67%, 28.81%, and 32.56%) were identified by 7, 9 and 11, respectively. Compound 7 showed mild inhibition against VEGFR-2 compared to sorafenib, the standard inhibitor.

The BuOH extract had the strongest cytotoxic and pro-apoptotic effects across most assays, with the lowest survival rate (30.11%), high caspase-3/7 (61.48%), high cytochrome c release (11.08 ng/mL), strong ROS (62.71%), and H2O2 production (5.11 µM), and the highest early and late apoptosis rates (26.19% and 29.47%). The findings demonstrate the potential of Beta Vulgaris chemical compounds as natural anticancer agents against breast cancer cells.

Furthermore, STX12 mRNA levels were significantly reduced following SF3A1 knockdown, indicating that SF3A1-mediated stabilization of STX12 contributes to apoptosis resistance in CRC cells. Collectively, our findings establish that SF3A1 promotes CRC progression by stabilizing STX12 mRNA and selectively inhibiting apoptosis in malignant cells, thereby identifying the SF3A1-STX12 regulatory axis as a novel and selective therapeutic target for CRC.

Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, with resistance to 5-fluorouracil (5-FU) representing a major therapeutic challenge...Combined TQ and 5-FU treatment did not produce synergistic cytotoxicity, as confirmed by Bliss independence analysis, but revealed distinct, cell line-dependent death programs. These findings demonstrate that TQ modulates cell death execution in a molecular context-dependent manner rather than enhancing 5-FU efficacy through pharmacological synergy.

Collectively, these findings support the effectiveness of a substitution-based strategy in improving parasporin fragments and underscore the therapeutic potential of peptide T104L-G108W as a novel anticancer candidate. Furthermore, this study provides preliminary evidence that natural biomolecules can be optimized through targeted modifications and rational combinations, establishing a framework for the development of sustainable and selective therapeutic approaches in cancer treatment.

The developed platform offered a robust and scalable approach for real-time functional phenotyping of immune effector responses, addressing a key gap in evaluating cell death mechanisms during immunotherapy development. By enabling the time-resolved quantification of tumor cell demise along with the mode of death, this dual-sensor system established a mechanistic framework for evaluation and rational design of safer and more effective next-generation immunotherapies.

Transcription factor target analysis demonstrated that a notable proportion of DEGs were likely regulated by GATA4. In conclusion, 3i-2012 decreases hepatoblastoma cell survival by disturbing cell cycle regulation in the tumor cells.

Importantly, compound 6 exhibited low inhibitory activity against monoamine oxidase A (MAO-A) and did not promote reactive oxygen species (ROS) generation, minimizing potential off-target effects. Together, these findings support the potential of compound 6 as a selective and effective candidate for antileukemia therapy.

In cerebellar organotypic slice cultures, PA 25 µM enhances axonal myelination and accelerates remyelination following lysolecithin-induced demyelination. These findings highlight the physiological relevance of low-dose PA in modulating OLs.

Cytotoxicity assays demonstrated markedly reduced IC50 values for NIO-CIS-VOR compared with free drugs: 1.8 µM vs. 4.47 µM (CIS) and 3.4 µM (VOR) in HT-29; 0.95 µM vs. 3.8 µM and 3.1 µM in A549; and 2.37 µM vs. 13.9 µM and 3.66 µM in PANC-1. Enhanced apoptosis and reduced colony formation further confirmed superior anticancer activity.In Conclusion the Co-loaded niosomes achieved efficient co-delivery, sustained release, and synergistic anticancer effects, highlighting NIO-CIS-VOR as a promising nanocarrier for combination cancer therapy.