Cisplatin enhances protein <i>O</i>‑GlcNAcylation by altering the activity of OGT, OGA and AMPK in human non‑small cell lung cancer cells

O‑GlcNAcylation is a dynamic and reversible post‑translational modification of proteins that modulated by O‑GlcNAc transferase (OGT) O‑GlcNAcase (OGA). Alterations in the protein expression O‑linked β‑N‑acetylglucosamine (O‑GlcNAc) can be induced multiple factors. However, little known effects chemotherapeutic agents on relevant molecular mechanisms cancer cells. In present study, to investigate whether cisplatin alters explore affects antitumor activity cisplatin, experiments were performed in vitro vivo. The results indicated treatment resulted an enhancement global levels H1299, Hep G2 MCF‑7 cells Cisplatin upregulated mRNA OGT OGA H1299 Moreover, significant enzymatic On contrary, activation decreased response exposure inhibited AMP‑activated kinase (AMPK) decreasing AMP/ATP ratio. study also revealed AMPK glutamine‑fructose‑6‑phosphate aminotransferase (isomerizing) 1 (GFAT1) phosphorylation subsequently promoted GFAT1. Cisplatin‑induced GFAT1 elevated production donor substrate, uridine 5‑diphospho‑N‑acetylglucosamine (UDP‑GlcNAc). alterations inhibition did not affect sensitivity lung cisplatin. whole, demonstrates enhances altering OGT,