Combining tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-producing oncolytic viruses with procaspase-3 activator (PAC-1) presents a promising therapeutic strategy, as TRAIL initiates apoptosis while PAC-1 amplifies caspase activity...This integrative approach provides mechanistic insight into tumor behavior while improving predictive accuracy, supporting the development of personalized therapeutic strategies for GCTs. The framework also offers broader applicability to other cancers with limited treatment options and heterogeneous responses.

By hybridizing this natural product scaffold with optimized structural elements from PAC-1, a reference procaspase-3 activator, 28 target compounds (K-01 ∼ K-28) were successfully synthesized...These results demonstrate that the hybrid molecular design strategy effectively combines the pharmacophoric advantages of both natural products and synthetic activators. The developed procaspase-3 activators exhibit improved therapeutic potential and represent promising candidates for further development as targeted anticancer agents modulating the caspase-3 activation pathway.

ImmuProgML offers a promising avenue for understanding the intricate relationship between tumors and the immune system, providing a machine learning framework for personalized cancer immunotherapy selections.

Our data show that PAC-1 modulates sunitinib-induced autophagy and blocks lysosomal trapping, potentiating sunitinib activity and increasing death of cancer cells. As both drugs are well-tolerated in patients, the data suggest evaluation of the PAC-1/sunitinib combination in a clinical trial of patients with PNET.

In addition, relative expression levels of von Willebrand Factor, β-TG, and iNOS and serum concentrations of PAC-1, β-TG, and iNOS were inhibited. Sodium ferulate can treat AAV by inhibiting NET release and platelet activation and reducing endothelial cell damage.

Drug sensitivity analysis further demonstrated that tumors with elevated pyrimidine metabolism displayed increased responsiveness to several chemotherapeutic agents, including BI-2536, JW-7-24-1, and PAC-1, suggesting that targeting pyrimidine metabolism may enhance treatment efficacy. In conclusion, pyrimidine metabolism plays a critical role in prostate cancer progression, influencing immune infiltration and drug sensitivity. Targeting this metabolic pathway offers a promising strategy for the development of new therapeutic approaches, particularly for overcoming drug resistance and improving outcomes in patients with advanced prostate cancer.

The study suggests that the S. nabateorum stem extract holds promise as a potent antimicrobial, antioxidant, and anticancer agent. It provides valuable insights for considering the extract as a substitute for chemotherapy and/or protective agents.

FHOD3 was overexpressed and negatively associated with survival rate in lung cancer patients. FHOD3 regulates cell proliferation, invasion, and apoptosis through the caspase-3-mediated signaling pathway. This study indicates that FHOD3 is an important gene contributing to the progression of lung cancer and might be a new drug target for the therapy of lung cancer.

The findings suggest that APX2009 sensitizes the MDA-MB-231 cells to doxorubicin in hypoxia by doxorubicin intracellular accumulation and caspases-3/7-mediated apoptosis.

Importantly, the clerodin did not exhibit cytotoxicity against human peripheral blood cells. These properties of clerodin make it a potential chemotherapeutic agent that can selectively induce apoptosis in leukemia-like cancer cells.

Med Sci Monit, 2017; 23: 2059-2064. DOI: 10.12659/MSM.901381.

SnuCalCpI15 was localized intracellularly in MDA-MB-231 breast cancer cells and suppressed tumor cell migration and invasion. These results demonstrate the potential of SnuCalCpI15 as a novel agent to prevent breast cancer metastasis.