| [1] PubMed ID: | 31766099 |
| Disease Name: | Stomach Neoplasms |
| Sample: | cell lines |
| Dysfunction Pattern: | Regulation[JAK2/STAT3 signaling pathway] |
| Validated Method: | qRT-PCR//MTT//Colony Formation Assay//Western Blot |
| Description: | 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. 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. |
| Causality: | Yes |
| Causal Description: | Downregulation of DC-SIGN significantly inhibited the proliferation, cell cycle progression, migration and invasion of GC cells in vitro. |
| Clinical-realted Application: | |
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