QPRT (Quinolinate Phosphoribosyltransferase)

ZIC2 may serve as a valuable prognostic and prognostic biomarker in pan-cancer, including CRC. ZIC2 may promote the colorectal cancer progression by upregulating QPRT.

Importantly, ADRB2/QPRT overexpression in hepatocytes, or nicotinamide administration, recovers CD8+ T cell function in stressed mice and reduces liver cancer progression. These findings identify a stress-responsive metabolic checkpoint in the liver that links the nervous system to immune surveillance and may be therapeutically targeted in liver cancers.

QPRT, RAB26, and SRPRB may be three potential novel prognostic biomarkers for TNBC and will provide potential guidance value for future research on TNBC.

These findings identify a novel role of LAT1 in promoting TNBC progression and chemo-resistance by amplifying the Warburg effect, positioning LAT1 as a promising therapeutic target for TNBC treatment.

This review represents the first article summarizing the current state of knowledge regarding the mechanisms of acquired drug resistance to NAMPT inhibitors with a particular focus on upregulation of the compensatory NAD+ production enzymes nicotinate phosphoribosyltransferase (NAPRT) and quinolinate phosphoribosyltransferase (QPRT), acquired mutations in NAMPT, metabolic reprogramming, and altered expression of the ATP-binding cassette (ABC) efflux transporter ABCB1. An understanding of how these mechanisms interact with the biology of each given cancer cell type to predispose to the acquisition of NAMPT inhibitor resistance will be necessary to develop strategies to optimize the use of these agents moving forward.

High-BCIS tumors exhibited enrichment in protein secretion and PI3K/AKT/mTOR pathways, associated with aggressiveness and therapy resistance. This study introduced the BCIS score, distinguishing invasion from non-invasion cells, linked to PI3K/AKT/mTOR pathways, offering insights into BRCA prognosis and tumor aggressiveness.

Therefore, understanding the distribution, cellular expression, and regulation of these enzymes and metabolites in the brain is critical for developing effective therapeutic strategies. In this review, we endeavor to describe these processes in detail.

In mouse transplantation models, depleting blood NAR by nutritional or genetic manipulations is synthetic lethal to tumors when combined with NAMPTi. Our findings provide a rationale for simultaneous targeting of NAR metabolism and NAMPT therapeutically in neuroendocrine carcinoma.

QPRT was associated with tumour immunity, especially in macrophages. QPRT may influence the occurrence and progression of breast cancer through the PI3K-AKT signalling pathway, Wnt signalling pathway, and cell cycle-related molecules.

The results indicated the up-regulation of TGM2 and HMGA2 in HCT116/OX-R10 cells with high OX-RI and down-regulation of FXYD3, LGALS4, and ECI2 in both cell types. Based on the results, TGM2, HMGA2, FXYD3, and LGALS4 genes are related to oxaliplatin-resistant CRC and may serve as novel therapeutic targets.

Immunohistochemical data obtained from the human protein atlas database demonstrated the protein expression of signature genes. This research may contribute to the identification of metabolic targets for BRCA and the optimization of risk stratification and personalized treatment for BRCA patients.