The effects of A549 and H1299 cell-derived exosomes on the proliferation and apoptosis of BEAS-2B cells

The effects of human non-small cell lung cancer A549 and H1299 cell-derived exosomes on BEAS-2B cell proliferation and apoptosis were investigated. Morphology and size of A549 and H1299 cell-derived exosomes were assessed using transmission electron microscopy and nanoparticle tracking analysis. BEAS-2B cell proliferation, apoptosis and SIRT7 protein expression were determined using CCK8, flow cytometry and Western blot. Transcriptome sequencing, GO analysis, and KEGG pathway analysis were performed. A549 and H1299 cell-derived exosomes demonstrated a microvesicle structure of bilayer membrane with a diameter of about 80 nm. Compared with control, these had no effect on BEAS-2B cell proliferation, but significantly promoted cell apoptosis, and decreased SIRT7 protein expression. Compared with control, A549 cell-derived exosomes have 20 differently expressed genes (10 upregulated, 10 downregulated); 1073 GO terms were enriched, while H1299 cell-derived exosomes have 112 differently expressed genes (80 upregulated, 32 downregulated); 3340 GO terms were enriched. For A549 cell-derived exosomes vs. control, the enriched pathways mainly included dorso-ventral axis formation, endocytosis, endometrial cancer, acute myeloid leukemia, and pathogenic Escherichia coli infection. For H1299 cell-derived exosomes vs. control, the enriched pathways mainly included influenza A, herpes simplex infection, measles, TNF signaling pathway, salmonella infection, and Hepatitis C. A total of 608,315 mutation sites were identified, including 553,800 single nucleotide polymorphism sites (SNP) and 54,515 Indel polymorphism sites. The SNP mutation sites were mainly concentrated in A->G, C->T, G->A and T->C. These findings suggested that A549 and H1299 cell-derived exosomes can promote BEAS-2B cell apoptosis by inhibiting SIRT7 expression.

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