XIAP (X-Linked Inhibitor Of Apoptosis)

Furthermore, transcriptomic analysis revealed that targeting CHCHD2 with CS-6 activates interferon signaling and significantly upregulates the tumor suppressor X-linked inhibitor of apoptosis (XIAP)-associated factor 1 (XAF1). In conclusion, these findings establish the mitochondrial CHCHD2-XAF1 axis as a key mediator of CS-6 activity, thereby highlighting CS-6 as a promising candidate for targeted therapy in NSCLC.

Comprehensive transcriptomic analysis revealed that heme synthesis inhibition induced OSGIN1 expression, leading to the release of cytochrome c and Smac from mitochondria into the cytoplasm. Therefore, heme synthesis inhibition induced leukemia apoptosis by activating the intrinsic apoptosis pathway.

In CSC-enriched cells, SATB2 inhibition was associated with increased sensitivity to cisplatin and pemetrexed, concomitant with reduced OCT4 and SOX2 expression. Collectively, these findings support SATB2 as a candidate therapeutic target in MPM and suggest that SATB2 suppression may enhance chemotherapy response when combined with standard agents.

This multicenter study showed the features of small bowel lesions among VEOIBD by VCE. Safety of VCE in VEOIBD patients have also been demonstrated.

YQJDF inhibits proliferation, invasion, and migration of NPC cells by inhibiting the AKT1/GLUT1 signaling pathway.

This study uses computational and database-based approaches to systematically explore potential associations between parabens and PCa, identifying 8 key genes that may mediate this association and providing a theoretical foundation for formulating safer preservative usage guidelines and exploring PCa prognostic markers. Importantly, the current findings are derived from in silico prediction and public database analysis, not from experimental verification involving paraben exposure controls. The study identifies potential correlations rather than verifying direct molecular mechanisms of parabens in PCa; thus, it generates valuable scientific hypotheses that require further validation via in vitro cell experiments, animal models, and human exposure cohort studies to confirm the actual molecular mechanisms linking parabens to PCa.

Lenvatinib exhibits potent anti-CRC activity with minimal systemic toxicity. Its therapeutic effects are mediated through ERK pathway inactivation, suppression of anti-apoptotic proteins, and induction of caspase-dependent apoptosis.

Here, we show that AZD5582 and AT406, potent antagonists of cellular inhibitor of apoptosis proteins 1 and 2 (cIAP1 and cIAP2) and X-linked inhibitor of apoptosis protein (XIAP), selectively eliminated HCT116 and RKO cells that had undergone senescence following treatment with a chemotherapeutic agent such as trifluridine, camptothecin, or doxorubicin. At physiological concentrations, TNFα sensitized non-senescent, proliferating cancer cells, but not TIS and nutlin-3a-induced senescent cancer cells, to apoptosis in the presence of IAP antagonists. Collectively, these findings suggest that IAP antagonists could serve as effective concomitant agents to TIS-inducing chemotherapy that promotes TNFα secretion within tumors, functioning not only as TNFα-independent senolytics but also as potentiators of TNFα-mediated apoptosis in adjacent non-senescent, proliferating cancer cells.

Peptide-5 potentially activates apoptotic signalling through modulating the Bcl-2/Bax mRNA expression. In summary, our study confirms that Peptide-5 is a highly potent and promising XIAP-targeted inhibitor for the treatment of cancer.

In XIAP deficiency, MDP-flow CD62L enabled faster functional analysis than MDP-flow TNF-α. These analyses are also useful for post-HCT functional assessment.

S-016-1348 holds drug like properties for its excellent oral bioavailability across species, promising pharmacokinetic properties, and well tolerated in preclinical safety evaluations with high safety margins. These findings highlight the translational potential of SMAC mimetic S-016-1348 as a monotherapy against solid tumors.

In addition to downregulation of anti-apoptotic proteins and upregulation of pro-apoptotic proteins, mTORC1 signaling was effectively hindered in the cells exposed to the drugs. Thus, induction of apoptosis by a combination of Metformin and DNC in MDA-MB-231 and MCF-7 cells is accompanied by the inhibition of anabolic pathways mediated by mTOR complex I.