Detail
LncRNA Name | MIAT |
Synonyms | MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT, FLJ25967 |
Region | GRCh38_22:26646428-26676475 Sequence |
Ensembl | ENSG00000225783 |
RefSeq | NR_003491 |
Circulating | ✘ |
Drug-resisitant | ✘ |
Prognostic | ✘ |
MiRNA | ✔ |
Variant | ✘ |
TF | ✘ |
Methylation | ✘ |
Cancer Name | colorectal cancer |
ICD-0-3 | C19.9 |
Methods | qPCR, Western blot, Luciferase reporter assay etc. |
Sample | colorectal cancer tissues, cell lines (HcoEpic, HT-29, SW480, and LOVO) |
Expression Pattern | up-regulated |
Function Description | MIAT was highly expressed in CRC tissues and cells.MIAT knockdown inhibited proliferation,migration and invasion and enhanced apoptosis of CRC cells.Further,we demonstrated that MIAT acted as a competing endogenous RNA for miR-132, antagonized its functions,and resulted in the de-repression of its target gene Derlin-1,which acted as an oncogene in promoting growth and metastasis of CRC cells.In LOVO and SW480 cells with si-MIAT, miR-132 inhibitor resulted in an increase of cell proliferation, migration and invasion and a decrease of cell apoptosis, which was partially abolished by transfection of Derlin-1 shRNA.Our data indicated that highly expressed MIAT was an oncogenic lncRNA that promoted the growth and metastasis of CRC through miR-132/Derlin-1 axis. |
Pubmed ID | 29686537 |
Year | 2018 |
Title | Long non-coding RNA MIAT promotes growth and metastasis of colorectal cancer cells through regulation of miR-132/Derlin-1 pathway. |
External Links |
Links for MIAT | GenBank HGNC lncrnadb Noncode |
Links for colorectal cancer | Omim Cosmic |
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