Basic Information
| LncRNA/CircRNA Name | uc002jit.1 |
| Synonyms | NA |
| Region | NA |
| Ensemble | NA |
| Refseq | NA |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | Drug | |||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | acute myeloid leukemia |
| ICD-0-3 | NA |
| Methods | Microarray, qPCR, Luciferase reporter assay etc |
| Sample | cell lines (KG1?, Kasumi-1, and HEK293) |
| Expression Pattern | down-regulated |
| Function Description | uc002jit.1 (D43770) was the most significantly downregulated. uc002jit.1 is a target gene of nuclear factor kappa B/RELA, RELA regulated uc002jit.1 transcription by binding to its promoter. Additionally, uc002jit.1 knockdown impaired the stability of poly (ADP-ribose) polymerase 1 (PARP1) mRNA, and then reduced PARP1 protein content and PARylation level upon DNA damage, thus inhibiting DNA damage repair in AML cells. Moreover, uc002jit.1 knockdown significantly inhibited AML cells proliferation and increased the sensitivity to chemotherapeutic drugs in vitro as well as in a mouse model in vivo. |
| Pubmed ID | 32259522 |
| Year | 2020 |
| Title | The Role of the Novel LincRNA uc002jit.1 in NF-kB-mediated DNA Damage Repair in Acute Myeloid Leukemia Cells |
External Links
| Links for uc002jit.1 | GenBank HGNC NONCODE |
| Links for acute myeloid leukemia | OMIM COSMIC |