XAF1 (XIAP Associated Factor 1)

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.

Transcriptome analysis revealed that combination treatment decreased the expression of pro-proliferative and migratory genes (e.g., PDPN, CDH3), while increasing the expression of anti-migratory (RND3) and pro-apoptotic genes (e.g., XAF1, SEMA3A). Thus, combination treatment significantly reduces tumor cell proliferation and migration; however, further studies on surviving cells are needed.

The hypothesis of Spanish immigrants carrying p.R337H to Paraguay was disproved. TP53 p.R337H neonatal testing in Paraguay is not recommended, except when there are families with Brazilian ancestry presenting cancer cases. Additional epidemiological studies are required to determine the likelihood of the identified prevalence of the XAF1 p.E134* allele (1/153) in NBs from Paraguay without TP53 p.R337H to present cancer risk. This study complements the first national initiative for the DNA screening of newborns aimed at mapping the TP53 p.R337H and XAF1 p.E134* variants in Paraguay (based on the regions of residence of the newborns).

This chapter provides a comprehensive overview of VSV engineering techniques, focusing specifically on the incorporation of the proapoptotic gene XAF1, along with detailed experimental procedures. The goal of these approaches is to increase the efficacy of VSV in antitumor immunity and other therapeutic domains.

In addition, gene network analysis highlighted CCNA2, CDK1, DDX58, DHX58, EXO1, GBP1, IFIH1, IFIT1, IFIT2, IFIT3, IRF7, ISIG15, MX1, OAS1, OAS2, PARP9, TOP2A and XAF1 as potential hub genes influencing the response of CCA cells to NDV LaSota strain. Our findings offer evidence supporting the promise of NDV-based therapies as potential strategies for eliminating CCA cells.

Animal experiments confirmed that the knockdown of TRIM47 inhibits tumor growth in vivo. Ultimately, TRIM47 promotes the ubiquitination and degradation of XAF1 and suppresses apoptosis and autophagy to promote the progression of HNSCC.

In a large Swedish early-stage breast cancer cohort, rs562556 homozygotes had a 22% risk of distant metastatic relapse at 15 years, whereas non-homozygotes had a 2% risk. Our findings reveal that a commonly inherited genetic alteration governs breast cancer metastasis and predicts survival-uncovering a hereditary basis underlying breast cancer metastasis.

In cancer cells exposed to interferon -γ, tumor necrosis factor -α, and etoposide, XAF1 is elevated and actively secreted through the unconventional endo-lysosomal trafficking pathway and the zinc finger 4 domain of XAF1 plays an essential for this secretion...XAF1 expression is associated with overall survival in T cell-enriched cancer patients and also correlates with prognosis in T cell-based immunotherapies. Together, our study identifies XAF1 as a novel secretory immune-modulatory tumor suppressor, illuminating the mechanistic consequence of its inactivation in tumorigenesis.

XAF1 expression is inversely correlated with TRIM28 expression in cancer cell lines and tumor tissues and more tightly associated with the survival of TRIM28-high versus TRIM28-low patients. Together, this study uncovers a novel mechanism by which XAF1 suppresses tumor malignancy and an important role for XAF1-TRIM28 interplay in governing stress response, illuminating the mechanistic consequence of its alteration during tumorigenic process.

Our results highlight the impact of hyperglycemic stress on the intestinal barrier function. This is of clinical relevance, as impaired barrier function has been observed in individuals with metabolic syndrome. Additionally, we demonstrate barrier protective effects of HA35 through its receptor layilin and modulation of cellular apoptosis under high glucose stress.

In conclusion, XAF1 overexpression impeded the advancement of NSCLC and repressed cisplatin resistance of NSCLC cells through inducing ER stress, which indicated that XAF1 might be a novel targeted-therapy for NSCLC.

ZBP1, XAF1, IFI44L, SOCS1, and PARP14 were relatively higher in cells with high PANscore. We developed a machine learning based Boruta algorithm for profiling PANoptosis related subgroups with in predicting survival and clinical features in the sepsis.