| [1] PubMed ID: | 30594388 |
| Disease Name: | Colorectal Neoplasms |
| Sample: | CRC tissues |
| Dysfunction Pattern: | Regulation[LINC00483/miR-204-3p/FMNL2 axial] |
| Validated Method: | Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//IHC//Transwell Assay |
| Description: | In the present study, we found a novel lncRNA, long intergenic non-protein coding RNA 483 (LINC00483), which was upregulated in CRC. LINC00483/miR-204-3p/FMNL2 axial might be a novel target in molecular treatment of CRC. |
| Causality: | Yes |
| Causal Description: | Functionally, we displayed that a knockdown of LINC00483 suppressed LOVO and HT29 cells proliferation and metastatic ability. |
| Clinical-realted Application: | We also illustrated that upregulated LINC00483 was correlated with poor clinicopathological features of patients with CRC. |
| [2] PubMed ID: | 33552987 |
| Disease Name: | Colorectal Neoplasms |
| Sample: | CRC biopsies |
| Dysfunction Pattern: | Regulation(HNF4α) |
| Validated Method: | qRT-PCR |
| Description: | LINC00483 was downregulated in CRC biopsies and metastases and its decreased levels were associated with severe clinical features.Moreover, we found that LINC00483 is potentially under negative control of transcription factor HNF4α. In conclusion, we propose that LINC00483 is a tumor suppressor in CRC that, through an RNA-RNA network, may control cell migration and participate in proliferation signaling. |
| Causality: | Yes |
| Causal Description: | Inhibition of the MAPK pathway and cell cycle arrest by starvation induced an upregulation of LINC00483, while the epithelial to mesenchymal transition activation by TGFβ-1 and IL-6 caused its down-modulation.Moreover, enforced expression of LINC00483 provoked a slowing down of cell migration rate without affecting cell proliferation. |
| Clinical-realted Application: | |
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