APAF1 (Apoptotic peptidase activating factor 1)

Sorafenib is a tyrosine kinase inhibitor (TKI) used to treat hepatocellular carcinoma (HCC), but this drug causes clinically significant toxicities in approximately 50% of patients...In addition, 6e attenuated the growth of HepG2 xenograft tumours in mice at a dose of 1 mg/kg for 3 weeks. Based on these results, this pyrimidine derivative could be an interesting compound for the design of new agents against HCC.

Our analyses reveal that Tan IIA regulates 13 core targets of Dox cardiotoxicity-with enrichment in pathways including canonical cancer and small cell lung cancer pathways-and that six of these targets exhibit high binding affinity for Tan IIA or Dox; notably, machine learning prioritized the histone methyltransferase EZH2 as the central target for Tan IIA's anti-TNBC activity, and we further show EZH2 is highly expressed in breast invasive carcinoma (BRCA) tissues and correlates positively with infiltration of immune cells (e.g., B cells, CD4⁺ T cells) and expression of immune-related molecules (including immunosuppressors and MHC-associated antigen-presenting molecules). Collectively, these findings demonstrate that Tan IIA may mitigate Dox cardiotoxicity via modulation of targets such as APAF1, AR, and TERT (and their associated signaling cascades) while targeting EZH2 to exert anti-TNBC effects, providing a mechanistic framework for repurposing Tan IIA to improve the safety and efficacy of Dox-based BC therapy.

This study is the first to demonstrate the potent anti-melanoma effect of atranorin. This demonstrates the natural compounds' effects on cell proliferation, cell cycle progression, and the suppression of metastasis. These findings emphasize the potential of atranorin as a novel natural compound for use in adjunctive or targeted melanoma therapy, and highlight the need for further preclinical and clinical evaluation.

QFG alleviates 5-FU-induced skeletal muscle fatigue in tumor-bearing mice by activating the AMPK/PGC-1α pathway and inhibiting mitochondria-dependent apoptosis in the gastrocnemius muscle.

Okh induced mitochondrial dysfunction, characterized by increased ROS production and loss of the mitochondrial membrane potential (ΔΨm), which led to the upregulation of APAF-1 and cytochrome C, activation of caspases-9 and -3, and initiation of apoptosis. The antitumor potential of Okh was confirmed in a 3D culture of MDA-MB-231 cells and was more significant than those of another A2BAR-targeted triterpene glycoside cucumarioside A0-1 and cisplatin.

Furthermore, more nuclear chromatin condensation and cell shrinkage were observed in the GDC-0152 treatment group. In conclusion, Smac could promote the degradation of IAPs, accelerate mitochondrial damage, induce Cyt-c oxidation and Apaf-1 recruitment during postmortem aging of Tibetan sheep meat, thus activating caspase-9/3, facilitating mitochondrial pathway apoptosis and effectively improving Tibetan sheep meat tenderness.

Additionally, BMS-202 treatment significantly elevated levels of pro-inflammatory cytokines, including IFN-γ and TNF-α, indicating a robust immune response (P<0.001). These findings suggest that BMS-202 effectively promotes apoptosis and enhances immune responses in lung cancer, underscoring its potential as a therapeutic agent in treating lung carcinogenesis.

These findings demonstrate that OTA selectively targets healthy immune cells rather than leukemia cells, highlighting its pronounced immunotoxic risk and the importance of caution when considering its effect in a hematological context. Although limited to in vitro models, this study underscores the necessity of further research to clarify the molecular basis of differential OTA sensitivity and its contribution to immunosuppression and hematological disease.

The SARM1-dependent BAX activation and the role of NF2 in axon degradation were validated in neuronal models of axon degeneration. Together, these findings reveal how SARM1-driven metabolic collapse rewires cell death execution, positioning BAX, MCL1, APAF1, NF2, and HERC4 as core effectors in a nonapoptotic degenerative pathway linking metabolic stress to neurodegeneration.

Importantly, systemic inflammation induced by LPS or bacterial infection is attenuated in Apip cKO mice but exacerbated in APIP-transgenic mice. Thus, our findings suggest that APIP is crucial in regulating both canonical and non-canonical inflammasomes, presenting a potential therapeutic target for inflammatory diseases.

In conclusion, AVEN, as a promising diagnostic and prognostic biomarker in LUAD, affected tumour progression, immune infiltration and apoptosis resistance through the lncRNA-AC012236.1/hsa-miR-30d-5p-AVEN axis. These findings provided new insights into the pathogenesis of LUAD and highlighted potential therapeutic targets for improving patient prognosis.

It was also shown to have a protective effect on the lungs against acute Methotrexate toxicity, preventing alveolar epithelial damage, congestion, inflammatory cell infiltration and alveolar degeneration despite the presence of mild fibrosis and interstitial edema. Alpha Pinene can be considered to be a highly valuable protective agent against Methotrexate-induced lung injury.