LncRNA Information | ||||||
---|---|---|---|---|---|---|
ID | EL0514 | Name | FTX | Aliases | LINC00182; MIR374AHG; NCRNA00182 | |
Species | Homo sapiens | Chromosome | X | Start site | 73946555 | |
End site | 74293574 | Chain | minus | Exon NO. | 7 | |
Assembly | Ensembl Release 89 | Class | lincRNA | NCBI accession | NR_028379 | |
Ensembl | ENSG00000230590 | Sequence |
Disease | |||||||||
---|---|---|---|---|---|---|---|---|---|
Disease | Method | Sample | Expression pattern | Dysfunction type | Description | PMID | Source | ||
hepatocelluar carcinoma | HCC tissues and cells; clinical analysis | HCC tissues and cells | up-regulated | N/A | pathway lncRNA Ftx/miR-545/RIG-I promotes HCC development by activating PI3K/Akt signaling | 26992218 | |||
hepatocelluar carcinoma | N/A | HBV-related HCC tissue | up-regulated | expression | The overexpression of miR-545/374a cluster located in the Ftx lncRNA is partially responsible for a poor prognosis, and monitoring sera levels of miR-545/374a may be a useful diagnostic marker for HCC. | 25299640 | |||
colorectal cancer | qPCR, knockdown etc | CRC and adjacent normal colorectal tissues, cell lines (HT-29, SW1116, SW480, COLO205) | up-regulated | expression | Long non-coding RNA FTX was significantly upregulated in colorectal cancer tissues, and low long non-coding RNA FTX expression was significantly correlated with differentiation grade, lymph vascular invasion, and clinical stage. Patients with high long non-coding RNA FTX showed poorer overall survival than those with low long non-coding RNA FTX. Multivariate analyses indicated that status of long non-coding RNA FTX was an independent prognostic factor for patients. Functional analyses showed that upregulation of long non-coding RNA FTX significantly promoted growth, migration, invasion, and increased colony formation in colorectal cancer cells. | 26629053 | Lnc2Cancer | ||
Function (not disease relevant) | |||||||||
---|---|---|---|---|---|---|---|---|---|
Methods | Sample/condition | Expression pattern | Dysfunction type | Description | PMID | Source | |||
N/A | N/A | Up-regulated | interaction | mutation cuasesalteration of transcript levels within the X-inactivation center and particularly important decreases in Xist RNA levels | 21118898 | ||||
Interaction | |||||||||
---|---|---|---|---|---|---|---|---|---|
Interaction target | Level of interaction | Type of interaction | Description | PMID | Source | ||||
Xist | RNA-RNA | regulation | The Ftx mutation, however, results in widespread alteration of transcript levels within the X-inactivation center (Xic) and particularly important decreases in Xist RNA levels. | 21118898 | |||||
RIG-I | RNA-Protein | regulation | Ectopic expression of RIG-I abrogated the effects of lncRNA Ftx or miR-545 on HCC cells. LncRNA Ftx/miR-545-mediated downregulation of RIG-I led to increased Akt phosphorylation in vitro and in vivo. | 26992218 | |||||
miR-545 , RIG-I | RNA-RNA | co-expression | MiR-545 was positively correlated with lncRNA Ftx expression. | 26992218 | |||||
PI3K/Akt signaling | N/A | regulation | The novel pathway lncRNA Ftx/miR-545/RIG-I promotes HCC development by activating PI3K/Akt signaling. | 26992218 | |||||