SNHG12 in cancer-associated fibroblast-derived extracellular vesicle induces macrophage-myofibroblast transition

Epigenomics. 2024 Dec-Dec;16(23-24):1415-1427. doi: 10.1080/17501911.2024.2430166. Epub 2024 Nov 20.

Abstract

Aims: To investigate mechanism of lncRNA SNHG12 induced macrophage-myofibroblast transition (MMT) in cancer-associated fibroblasts (CAFs)-derived extracellular vesicles (EVs) in non-small cell lung cancer (NSCLC).

Method: CAFs EVs were isolated from human NSCLC tissue and adjacent cancerous tissue (n = 3), and their morphology and particle size were evaluated. Macrophages and MMT cells with different phenotypes were detected, and the binding relationship of lncRNA SNHG12, miR-181a-5p, and Smad3 was verified.

Result: LncRNA SNHG12 derived from CAFs-EVs promoted the transformation of M2 macrophages into MMT. In addition, lncRNA-SNHG12 increased the expression of Smad3 which was significantly upregulated in MMT through sponge of miR-181a-5p.

Conclusion: LncRNA SNHG12 derived from CAFs-EV induced MMT in NSCLC.

Keywords: CAFs-EVs; MMT; Macrophages; NSCLC; Smad3; lncRNA SNHG12; miR-181a-5p.

MeSH terms

  • Cancer-Associated Fibroblasts* / metabolism
  • Cancer-Associated Fibroblasts* / pathology
  • Carcinoma, Non-Small-Cell Lung* / genetics
  • Carcinoma, Non-Small-Cell Lung* / metabolism
  • Carcinoma, Non-Small-Cell Lung* / pathology
  • Cell Line, Tumor
  • Extracellular Vesicles* / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lung Neoplasms* / genetics
  • Lung Neoplasms* / metabolism
  • Lung Neoplasms* / pathology
  • Macrophages* / metabolism
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Myofibroblasts* / metabolism
  • RNA, Long Noncoding* / genetics
  • Smad3 Protein* / genetics
  • Smad3 Protein* / metabolism

Substances

  • RNA, Long Noncoding
  • MicroRNAs
  • Smad3 Protein
  • SNHG12 long non-coding RNA, human
  • SMAD3 protein, human

Grants and funding

This paper was not funded.