The NR3C2-SIRT1 signaling axis promotes autophagy and inhibits epithelial mesenchymal transition in colorectal cancer

Cell Death Dis. 2025 Apr 14;16(1):295. doi: 10.1038/s41419-025-07575-3.

Abstract

Colorectal cancer (CRC) is one of the most aggressive and lethal cancers with a complex pathogenesis, there is an urgent need to find new drug therapeutic targets. This study highlights the important role of the NR3C2-SIRT1 signaling axis in the metastasis mechanism of CRC. Our findings revealed that the expression of NR3C2 in CRC tissues was lower than that in adjacent non-cancerous tissues, and was negatively correlated with N stage by bioanalysis, IHC, western blot and qRT-PCR. NR3C2 overexpression / knockdown can significantly inhibit / promote the migration and invasion of CRC cells, at the same time inhibit / promote EMT. Mechanically, the regulatory molecule SIRT1 was identified by RNA-seq, bioinformatics analysis, western blot and ChIP. SIRT1 was also involved in the metastasis process of CRC, and NR3C2 was found to regulate the expression of LC3B and SQSTM1/p62 in a SIRT1-dependent manner. Therefore, NR3C2 forms a signaling axis with SIRT1, which can directly promote autophagy and inhibit EMT process in vivo and in vitro. Collectively, our findings suggest that NR3C2 - SIRT1 signal axis promote autophagy and inhibit EMT, ultimately inhibits lung metastasis of CRC.

MeSH terms

  • Animals
  • Autophagy* / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Colorectal Neoplasms* / genetics
  • Colorectal Neoplasms* / metabolism
  • Colorectal Neoplasms* / pathology
  • Epithelial-Mesenchymal Transition* / genetics
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Receptors, Glucocorticoid* / genetics
  • Receptors, Glucocorticoid* / metabolism
  • Receptors, Mineralocorticoid
  • Signal Transduction
  • Sirtuin 1* / genetics
  • Sirtuin 1* / metabolism

Substances

  • Sirtuin 1
  • SIRT1 protein, human
  • NR3C2 protein, human
  • Receptors, Glucocorticoid
  • Receptors, Mineralocorticoid