| [1] PubMed ID: | 31557619 |
| Disease Name: | Colorectal Neoplasms |
| Sample: | cell lines |
| Dysfunction Pattern: | Regulation[JAK/STAT3 Signaling] |
| Validated Method: | ChIP//Western Blot//Co-IP//CCK8//qRT-PCR//RIP//Luciferase Report Assay//Transwell Assay//IF |
| Description: | Interestingly, a significant overexpression of ITIH4-AS1 was observed in CRC cell lines relative to normal NCM460 cells. Additionally, we explained that ITIH4-AS1 upregulation in CRC was attributed to downregulation or even depletion of RE1 silencing transcription factor (REST), a presently identified transcriptional repressor for ITIH4-AS1. Meanwhile, the contribution of ITIH4-AS1 to CRC development was validated to rely on the activation of the JAK/STAT3 pathway. More importantly, we verified that FUS interacted with both ITIH4-AS1 and STAT3, and that ITIH4-AS1 evoked nuclear translocation of phosphorylated (p)-STAT3 in CRC through recruiting FUS. In summary, our findings unveiled for the first time that REST downregulation-enhanced ITIH4-AS1 exerts pro-tumor functions in CRC through FUS-dependent activation of the JAK/STAT3 pathway, implying that targeting ITIH4-AS1 may be a novel effective strategy for CRC therapy. |
| Causality: | Yes |
| Causal Description: | Also, we investigated the facilitating role of ITIH4-AS1 in CRC cell growth and metastasis both in vitro and in vivo. |
| Clinical-realted Application: | |
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