BID (BH3 Interacting Domain Death Agonist)

The ability to downregulate these cytokines was close to that of aspirin and stronger than that of low concentration LR-AFY02L. By controlling the NF-κB and apoptosis pathways, LR-AFY02 can help reduce intestinal inflammation and prevent the growth of intestinal tumors. These findings suggested that LR-AFY02 may have regulatory effects on colon cancer in mice and merits additional study.

BID, specifically the BID-EL isoform, serves as a prognostic and diagnostic biomarker in COAD, highlighting the need for further research on its potential as a therapeutic target in this disease.

Small-molecule inhibitors such as ABT-737 and Navitoclax, kinase inhibitors targeting NF-κB (Nuclear Factor kappa-light-chain-enhancer of Activated B Cells) and JAK/STAT (Janus Kinase/Signal Transducer and Activator of Transcription) pathways, and natural compounds including fucoxanthin, peridinin, and thymoquinone have demonstrated the ability to overcome apoptosis resistance in preclinical models. Recent strategies combining MCL-1 inhibitors with antiretroviral therapy or immune checkpoint blockade further highlight the translational potential of targeting BCL-2 pathways. Collectively, the evidence positions the BCL-2 family as a critical determinant of deltaretroviral persistence and leukemogenesis, and as a promising therapeutic axis for the development of novel treatments for HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) and BLV-associated leukosis.

NCA demonstrates significant anti-tumor activity against gastric cancer cells both in vitro and In vivo, suggesting its potential as a therapeutic agent. These findings suggest that NCA suppresses gastric cancer via apoptosis and cell cycle arrest and warrants further preclinical and clinical evaluation as a potential therapeutic strategy for gastric cancer.

This study provides compelling evidence that NCA inhibits HCC cell growth and migration both in vitro and in vivo through the induction of apoptosis and cell cycle arrest. Transcriptomic analysis reveals that NCA induces widespread changes in transcriptional networks and metabolic pathways within HCC cells, highlighting its potential as a promising therapeutic strategy for HCC.

These findings support the hypothesis that cantharidin induces apoptosis via both intrinsic and extrinsic pathways, as well as through suppression of the JAK2-STAT3 axis. Our results reveal that cantharidin holds significant promise as a multi-target therapeutic candidate for NBL, justifying additional in vivo validation and clinical translation efforts.

Moreover, it was significantly downregulated VEGF, survivin and Bcl2 while, it was significantly upregulated BAX, BAK and BID. In conclusion, sea cucumber Ps extract may be an effective chemotherapeutic agent against HCC.

Thus, CAE might be a novel potential candidate for the treatment of gastric cancer. The online version contains supplementary material available at 10.1007/s13205-025-04318-1.

Understanding Bid's signaling pathways offers valuable insights into host-virus interactions and the pathogenesis of infections. This knowledge may facilitate the development of novel therapeutic approaches to combat virus-associated diseases effectively.

The mRNA and protein expression of NCoR1 and DLK1 in siRNA-mediated transfection supported the reduced proliferation in endometrial cancer cells by interfering with certain pathways like Notch, MAPK, SWI/SNF, and NF-κB, which have crucial roles in the grade of receptor to the histone remodeling. With these findings, the study recommends exploring the possible role and interactions of NCoR1 and DLK1, signaling pathways that favor the progression of endometrial cancer.

Based on our existing research results and the findings of previous researchers, we infer that HERV-W env acts as a bridge in the onset and progression of schizophrenia. Furthermore, HERV-W env may serve as a potential target for the clinical treatment of schizophrenia, suggesting that monoclonal antibody therapy targeting HERV-W env could represent a novel approach to managing this disease.

Raddeanin A treatment increased Ras, Raf phosphorylation, MEK phosphorylation, NKG2D, NKp44 and NKp30 expression in KHYG-1 cells. Collectively, our data indicate that Raddeanin A enhances the cytotoxic activity of NK cells against different cancer cells.