DC-SIGN mediates gastric cancer progression by regulating the JAK2/STAT3 signaling pathway and affecting LncRNA RP11-181G12.2 expression - 30/11/19
, Heya Na a, c, 1 , Lijie Xu a , Xinsheng Zhang b , Zhen Feng b , Xu Zhou a , Jingyi Cui a , Jingbo Zhang a , Fang Lin a , Shiqing Yang a , Fangxia Yue a , Haithm Mousa a , Yunfei Zuo a, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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| pages | 10 |
| Iconographies | 7 |
| Vidéos | 0 |
| Autres | 0 |
Highlights |
• | DC-SIGN is associated with gastric cancer progression. |
• | There is a negative correlation between DC-SIGN expression and lncRNA RP11-181G12.2 expression. |
• | DC-SIGN can activate the JAK2/STAT3 signaling pathway in gastric cancer cells. |
Abstract |
Background |
The molecular mechanisms of gastric cancer (GC) development are very complicated. Recent studies revealed that DC-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN)-related protein (DC-SIGNR) is involved in colon cancer and GC biological processes. However, the exact roles of DC-SIGN in GC remain unrevealed.
Methods |
DC-SIGN overexpression and knockdown experiments were performed by using DC-SIGN shRNA or DC-SIGN plasmid to investigate the biological roles of DC-SIGN in proliferation, cell cycle progression, migration and invasion of GC cells in vitro. Furthermore, the lncRNA profiles of SGC-7901 cells with control shRNA and DC-SIGN shRNA were generated by using microarray analysis. Mechanistically, the relationship between DC-SIGN, RP11-181G12.2 and the JAK2/STAT3 signaling pathway was then investigated using qRT-PCR and western blot assays. Additionally, we analyzed DC-SIGN and RP11-181G12.2 expression levels in GC specimens based on the Cancer Genome Atlas database.
Results |
In this study, the results showed that DC-SIGN was highly expressed in GC cells and significantly correlated with advanced clinical stage and lymphatic metastasis. Downregulation of DC-SIGN significantly inhibited the proliferation, cell cycle progression, migration and invasion of GC cells in vitro. The reverse results could partly be seen with the upregulation of DC-SIGN. Mechanistically, knockdown of DC-SIGN inactivated the JAK2/STAT3 signaling pathway, and overexpression of DC-SIGN activated the JAK2/STAT3 signaling pathway. In addition, through LncPath microarray analysis, we identified a lncRNA, RP11-181G12.2, that was significantly upregulated after knockdown of DC-SIGN; this was also confirmed by qRT-PCR. Furthermore, RP11-181G12.2 knockdown enhanced DC-SIGN expression in GC cells, further activating the JAK2/STAT3 signaling pathway. In contrast, DC-SIGN overexpression suppressed RP11-181G12.2 expression.
Conclusions |
Our study suggests that DC-SIGN might be involved in the progression of GC by regulating the JAK2/STAT3 signaling pathway and affecting lncRNA RP11-181G12.2 expression.
Le texte complet de cet article est disponible en PDF.Abbreviations : DC-SIGN, GC, DC-SIGNR, LSECtin, DCs, PRR, CEA, lncRNAs, STAT3, JAK2, FPKM
Keywords : DC-SIGN, Gastric cancer, JAK2/STAT3, lncRNA
Plan
Vol 121
Article 109644- janvier 2020 Retour au numéro
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