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Abstract Nicotinamide adenine dinucleotide (NAD+) replenishment sensitizes tumors to immunotherapy. However, chemotherapy-induced NAD+ metabolic reprogramming remains poorly understood. Here, we show that chemotherapy induces a macrophage-dependent IL-1β inflammatory response and NAD+ metabolic reprogramming, thereby conferring chemoresistance via CD44.
Introduction Nicotinamide adenine dinucleotide (NAD + ) is a key mediator of energy metabolism and signal transduction pathways ( ; Chiarugi et al., 2012 Chiarugi A. Dölle C. Felici R. Ziegler M. The NAD metabolome--a key determinant of cancer cell biology. ).
In metastatic niche, CAFs have been demonstrated to actively participate in the tumor metastasis progression8. Similar results were observed in tissues of lung metastasis from HCC patients (Supplementary Fig. 1a) and in liver cancer cells in mice models (Supplementary Fig. 1b), according to the high expression of ?-SMA, which is the most effective marker. Thus, it is very important to get a further understanding on CAFs activation caused by tumor cells.
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