Related LncRNAs |
ID |
lncRNA Name |
Disease |
Method |
Sample |
Expression pattern |
Dysfunction type |
Description |
PMID |
Source |
EL0276 |
CCAT1 |
acute myeloid leukemia |
gain- and loss-of-function analysis |
French-American-British M4 and M5 subtypes of adult AML patients |
up-regulated |
N/A |
repressed monocytic differentiation and promoted cell growth of HL-60 |
26923190 |
|
EL0282 |
CCDC26 |
acute myeloid leukemia |
microarray, qPCR, Western blot etc. |
cell lines (HL-60, K562 etc.) |
up-regulated |
interaction |
We found that CCDC26 transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. We suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression.A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered. |
25928165 |
Lnc2Cancer
|
EL0289 |
CDKN2B-AS1 |
acute myeloid leukemia |
qPCR, knockdown etc. |
cell lines (KG-1, Kasumi-1) |
up-regulated |
N/A |
We found an inverse relation between p15 antisense (p15AS) and p15 sense expression in leukaemia. A p15AS expression construct induced p16 silencing in cis and in trans through heterochromatin formation but not DNA methylation; the silencing persisted aftp15AS was turned off, although methylation and heterochromatin inhibitors reversed this process. Moreover, 11 out of 16 patient samples (69%) showed relatively increased expression of p15AS and downregulated p15 expression (6/11 in acute myeloid leukaemia and 5/5 in acute lymphoblastic leukaemia). In contrast, 16 normal controls showed high expression of p15 but relatively low expression of the p15AS. Additionally, the two acute myeloid leukaemia lines, which displayed high p15AS and low p15 expression.on. |
18185590 |
Lnc2Cancer
|
EL0578 |
HOTAIR |
acute myeloid leukemia |
qPCR, knockdown etc. |
bone marrow, cell lines (HL60, K562) |
up-regulated |
expression |
We found that HOTAIR is significantly upregulated in de novo AML patients compared with those of AML-CR patients and normal controls; the reduction of HOTAIR by small interfering RNA (siRNA) repressed the proliferation of HL-60 and K562; the higher expression level of HOTAIR in AML patients was significantly correlated with NCCN high risk group. |
26261618 |
Lnc2Cancer
|
EL0578 |
HOTAIR |
acute myeloid leukemia |
qPCR, Western blot, knockdown, RIP etc. |
cell lines |
up-regulated |
interaction |
We report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Clinically, AML patients with higher HOTAIR predicted worse clinical outcome compared with those with lower HOTAIR. Importantly, HOTAIR knockdown by small hairpin RNA inhibited cell growth, induced apoptosis, and decreased number of colony formation. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. |
25979172 |
Lnc2Cancer
|
EL0580 |
HOTAIRM1 |
acute myeloid leukemia |
N/A |
241 AML patients, 215 intermediate-risk AML (IR-AML) patients |
N/A |
interaction |
In 215 IR-AML patients, high HOTAIRM1 expression was independently associated with shorter overall survival (OR:2.04;P = 0.001), shorter leukemia-free survival (OR:2.56; P < 0.001) and a higher cumulative incidence of relapse (OR:1.67; P = 0.046). HOTAIRM1 was overexpressed in NPM1-mutated AML (P < 0.001) and within this group retained its prognostic value (OR: 2.21; P = 0.01). miR-196b and HOTAIRM1 in combination as a prognostic factor can classify patients as high-, intermediate-, or low-risk (5-year OS: 24% vs 42% vs 70%; P = 0.004). |
26433964 |
|
EL0619 |
IRAIN |
acute myeloid leukemia |
qPCR, Northern blot, in vitro knockdown, ChIP etc. |
blood, cell lines (K562, KG-1, KG-1a, HL60, TF1) |
down-regulated |
interaction |
We demonstrate that this lncRNA interacts with chromatin DNA and is involved in the formation of an intrachromosomal enhancer/promoter loop. In addition, IRAIN was downregulated both in leukemia cell lines and in blood obtained from high-risk AML patients. Activating the IGF1R gene, lead to growth advantage and tumor progression. |
25092925 |
Lnc2Cancer
|
EL0861 |
MEG3 |
acute myeloid leukemia |
MSP etc. |
bone marrow |
down-regulated |
epigenetics |
MEG3 hypermethylation occurred in 15 MDS patients (34.9%), and in 20 AML patients (47.6%). |
19595458 |
LncRNADisease Lnc2Cancer
|
EL1173 |
RUNX1 |
acute myeloid leukemia |
qPCR, RNA-ChIP etc. |
bone marrow, cell lines (KG-1, KG-1a, Kasumi-1, K562) |
up-regulated |
regulation |
RUNXOR utilizes its 3'-terminal fragment to directly interact with the RUNX1 promoter and enhancers and participates in the orchestration of an intrachromosomal loop. The 3' region of RUNXOR also participates in?long-range interchromosomal interactions with chromatin regions that are involved in multiple RUNX1 translocations. |
24752773 |
LncRNADisease Lnc2Cancer
|
EL1431 |
UCA1 |
acute myeloid leukemia |
RNA-seq, qPCR, in vitro knockdown, RIP etc. |
cell lines(K562 , CEBPA, CEBPA-P30, K562etc.) |
up-regulated |
interaction |
In this study, we identified the oncogenic urothelial carcinoma associated 1 (UCA1) lncRNA as a novel target of the C/EBPα-p30. While wild-type C/EBPα represses, C/EBPα-p30 can induce UCA1 transcription. Notably, we also show that UCA1 expression increases in cytogenetically normal AML cases carrying biallelic CEBPA mutations.Thus, we identified, for the first time, an oncogenic lncRNA functioning in concert with the dominant negative isoform of C/EBPα-p30 in AML. |
26053097 |
Lnc2Cancer
|
EL1456 |
WT1-AS |
acute myeloid leukemia |
qPCR etc. |
bone marrow tissue |
differential expression |
epigenetics |
The incidence of WIT-1 methylation in primary refractory AML was significantly higher than that noted in chemosensitive AML. |
10340388 |
LncRNADisease Lnc2Cancer
|
EL1456 |
WT1-AS |
acute myeloid leukemia |
qPCR etc. |
Bone marrow |
up-regulated |
Interaction |
In AML, there is often abnormal splicing of WT1-AS, which may play a role in the development of this malignancy. |
17940140 |
LncRNADisease Lnc2Cancer
|
|