Disease |
Disease |
Method |
Sample |
Expression pattern |
Dysfunction type |
Description |
PMID |
Source |
colorectal cancer |
microarray, qPCR, knockdown etc. |
cell lines (HCT116, HT29, LS174T etc.) |
up-regulated |
N/A |
In colorectal cancer cells, we demonstrate that treatment with insulin and insulin-like growth factors (IGF) repressed CRNDE nuclear transcripts, including those encompassing gVC-In4. These repressive effects were negated by use of inhibitors against either the PI3K/Akt/mTOR pathway or Raf/MAPK pathway, suggesting CRNDE is a downstream target of both signaling cascades. |
24184209 |
Lnc2Cancer
|
colorectal cancer |
qPCR etc. |
CRC tissue |
up-regulated |
expression |
An uncharacterized gene locus (Chr16:hCG_1815491), now named colorectal neoplasia differentially expressed (gene symbol CRNDE), is activated early in colorectal neoplasia. |
22393467 |
LncRNADisease Lnc2Cancer
|
glioma |
qPCR, Western blot, ChIP, Flow cytometry assay etc. |
glioma tissue, cell lines(U87MG, U251) |
up-regulated |
expression |
Overexpression of specific CRNDE transcript promotes cell growth and migration in vitro while knockdown of CRNDE expression manifests a repressive function during these cellular processes. Mechanistic studies further revealed that histone acetylation in the promoter region might account for the upregulation of CRNDE, and the level of CRNDE expression could be modulated by mammalian Target of Rapamycin (mTOR) signaling in glioma. |
25813405 |
Lnc2Cancer
|
colorectal cancer |
quantitative real-time |
142 CRC tissues and 142 paired adjacent nontumorous tissues |
up-regulated |
N/A |
upregulation of lncRNA CRNDE-h was significantly correlated with large tumor size |
27042112 |
|
|