KYNU (Kynureninase)

A prognosis model based on fatty acid metabolism can serve as an effective tool for assessing the prognosis of LUAD patients. Due to incomplete clinical information in some datasets, comprehensive subgroup analyses could not be performed.

In particular, elevated KAT and KYNA levels demonstrated high diagnostic performance. These findings suggest that a panel of kynurenine pathway metabolites could aid in the early, non-invasive detection of pituitary adenomas.

Further, PTSK@CRM reduces the infiltration of immunosuppressive cells, thereby reversing ITME to improve the therapeutic efficacy of αPD-1. Overall, this immune-metabolic therapeutic strategy provides a potential route for remodeling ITME to enhance tumor immunotherapy.

Our explored the changes induced by trastuzumab resistance in terms of metabolite abundance and gene transcription levels associated with tryptophan metabolism. Furthermore, this work provided new insights into novel diagnostic biomarkers and prediction models of trastuzumab resistance in HER2-positive breast cancer patients.

Within the HRG cohort, both cisplatin and gemcitabine demonstrated significant sensitivity. This study identified four prognostic genes in LUAD and examined their associated mechanisms of action, which may contribute to the development of novel treatment strategies. The integration of immune characterization with drug sensitivity analysis offers valuable insights for stratified therapy.

Integrative mapping of genes and metabolites to the KEGG enzyme database highlighted L-tryptophan interactions, with KYNU, KMO, KYAT3, and AADAT as the most representative relationships. These results provide a quantitative overview of MDV-induced transcriptional and metabolic perturbations, suggesting that hosts may counteract viral infection and tumor progression by suppressing cellular metabolism to potentiate immune responses.

This study identifies five propionate metabolism-related genes (LDHA, KYNU, SLC2A1, CFTR, MAOB) that may influence LUAD prognosis, providing a scientific foundation for further mechanistic investigations and potential clinical applications. (Liu C, He L, Peng Z, Luo J, A New Prognostic Model for Lung Adenocarcinoma According Propionate Metabolism Related Genes: A Comprehensive Bioinformatic Study, Abstract Book of MEDLIFE2024 & ICBLS2024 (ISBN:979-8-88599-099-8), 2024.).

This study elucidated the unique metabolic characteristics and molecular signatures of NPC, clarified how molecular changes regulate gene expression, and provided new potential targets for prognostic evaluation and precision treatment of NPC.

In vitro studies in GBM cell lines (U87, U251, T98G) assessed the effects of KYNU silencing and treatment with an HDAC6 inhibitor (tubastatin) and a BET inhibitor (apabetalone) on gene expression and cell viability... Our findings establish the KYNU-HDAC6-complement axis as a critical regulatory pathway in GBM. Targeting KYNU-mediated complement activation through combined epigenetic approaches-such as HDAC6 and BET inhibition-represents a promising strategy to overcome complement-driven resistance in GBM therapy.

The results of the present study further elucidated the molecular processes underlying PDAC and highlight the crucial importance of manganese metabolism in its development. These biomarkers may provide significant prognostic insights and facilitate the advancement of targeted therapeutic strategies for PDAC.

M2-secreted KYNU promotes the malignant behavior and stemness remodeling of EC via the SOD2-mtROS-ERO1α-UPRER axis and establishes a positive feedback loop. Thus, KYNU is a potential therapeutic target for EC treatment.

Among patients with high IDO1/TDO2 expression, high KYNU levels were significantly associated with better prognosis (p = 0.03, HR 0.43, 95 %CI 0.16-0.82). These findings suggest that the immunohistochemical evaluation of IDO1, TDO2 and KYNU in BCa tissue samples is feasible, providing a triple-marker approach for prognostic assessment and may guide immuno-oncology trials targeting the kynurenine pathway.