The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
| Autor: | Sho Hangai, Hideyuki Yanai, Shotaro Eto, Daiki Kato, Ryohei Nishimura, Takayuki Nakagawa |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Science
Cell Gene Expression Inflammation Article Dinoprostone Cell Line Mice Immune system Dogs Cell Line Tumor Gene expression Cell death and immune response medicine Extracellular Animals RNA Messenger Multidisciplinary Chemistry Tumor Necrosis Factor-alpha Macrophages medicine.anatomical_structure RAW 264.7 Cells Cell culture Cyclooxygenase 2 Cancer research Medicine Tumor necrosis factor alpha medicine.symptom Chemokines Intracellular |
| Zdroj: | Scientific Reports, Vol 11, Iss 1, Pp 1-13 (2021) Scientific Reports |
| ISSN: | 2045-2322 |
| Popis: | Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with inflammation and cancer pathogenesis. Thus, elucidating the role of damage-associated molecules in inducing sterile immune responses is crucial. In this study, we show that prostaglandin E2 (PGE2) is produced in the supernatants from several types of canine necrotic tumor cell lines. Inhibition of PGE2 production by indomethacin, a potent inhibitor of cyclooxygenase (COX) enzymes, induces the expression of tumor necrosis factor (Tnf) mRNA in the necrotic tumor cell supernatants. These results comply with the previous observations reported in mouse cell lines. Furthermore, comprehensive ribonucleic acid-sequencing (RNA-seq) analysis revealed that three categories of genes were induced by the damage-associated molecules: (i) a group of PGE2-inducible genes, (ii) genes that promote inflammation and are suppressed by PGE2, and (iii) a group of genes not suppressed by PGE2. Collectively, our findings reveal the hitherto unknown immune regulatory system by PGE2 and damage-associated molecules, which may have clinical implications in inflammation and cancer. |
| Databáze: | OpenAIRE |
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