IDDF2022-ABS-0018 Nicotinamide mononucleotide inhibits human hepatocarcinoma cell proliferation in vitro by activating SIRT1/MTOR signaling pathway

Background

To investigate the antitumor effect of Nicotinamide mononucleotide (NMN) on hepatocellular carcinoma (HCC) in culture and the underlying mechanisms of the effect.

Methods

Human hepatocellular carcinoma cell line HepG2 were randomly divided into HepG2 group, NMN (5 μM) supplementation group, and SIRT1 inhibitor & NMN treatment group. Cell proliferation was investigated by using MTT assay and Edu assay after the administration of NMN for 48 h. And then RNA and proteins were extracted and analysed by qPCR and western blot respectively.

Results

MTT and Edu results showed that exposure to NMN (5 μM) for 48 h significantly inhibited cell growth, decreased the proliferation of Human hepatocellular carcinoma cell lines and led to generally poor performance status of the cells (IDDF2022-ABS-0018 Figure 1. NMN significantly inhibited the cell growth of HepG2). Furthermore, the qPCR and Western blot results indicated that the SIRT1 activation by NMN could inhibit the mTOR signal and the SIRT1 inhibition by nicotinamide (SIRT1 inhibitor) notably impaired the effect of NMN (IDDF2022-ABS-0018 Figure 2. NMN inhibited mTOR signal and nicotinamide impaired the effect of NMN). Present data suggest that SIRT1/mTOR signaling is crucial for the growth of hepatocellular carcinoma cells and NMN plays an important role in the modulation of the signaling.

Conclusions

Nicotinamide mononucleotide inhibits hepatocellular carcinoma cell growth in vitro by regulating the SIRT1/mTOR signaling pathway.