Disease |
Disease |
Method |
Sample |
Expression pattern |
Dysfunction type |
Description |
PMID |
Source |
hepatocelluar carcinoma |
dual luciferase reporter gene assays |
HCC tissue specimens, mouse xenograft model |
up-regulated |
interaction |
Tthe miR-192/-204-HOTTIP axis might be an important molecular pathway during hepatic cell tumorigenesis. |
26710269 |
|
pancreatic cancer |
microarray, qPCR, Western blot, knockdown etc. |
cell lines (Panc1, ASPC1, BxPC3 etc.) |
up-regulated |
interaction |
HOTTIP is expressed in pancreatic cancer cell lines and knockdown of HOTTIP by RNA interference (siHOTTIP) in Panc1 pancreatic cancer cells decreased proliferation, induced apoptosis and decreased migration. HOTTIP functions in pancreatic cancer cells are due, in part, to regulation of some HOX genes including HOXA10, HOXB2, HOXA11, HOXA9 and HOXA1. |
25912306 |
Lnc2Cancer
|
pancreatic ductal adenocarcinoma |
microarray, qRT-PCR |
eight human pancreatic ductal adenocarcinoma (PDAC) tissues and four pancreatic tissues. |
up-regulated |
expression |
Functionally, HOTTIP silencing resulted in proliferation arrest by altering cell-cycle progression, and impaired cell invasion by inhibiting epithelial-mesenchymal transition in pancreatic cancer. HOTTIP promotes cell proliferation, invasion, and chemoresistance by modulating HOXA13. Therefore, the HOTTIP/HOXA13 axis is a potential therapeutic target and molecular biomarker for PDAC. |
25889214 |
|
prostate cancer |
microarray, RNA-seq, qPCR, Northern bolt, knockdown etc. |
prostate cancer tissue, cell lines (LNCaP, CWR22Rv1, PC3 etc.) |
down-regulated |
N/A |
Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. |
23728290 |
Lnc2Cancer
|
lung cancer |
N/A |
lung cancer cell line A549 and NCI-H446; tissue of lung cancer |
up-regulated |
expression |
Initially, we found that expression of HOTTIP was significantly elevated in 20 cases of lung cancer.Tumor growth in vivo was also suppressed after depletion of HOTTIP in a mouse model of lung cancer. Moreover, depletion of HOTTIP caused cell cycle arrest in G0/G1 phase and induced significant cell apoptosis. |
26265284 |
|
hepatocelluar carcinoma |
N/A |
N/A |
N/A |
expression |
Currently, upregulated HOTTIP and HOXA13 expressions were associated with the prognosis and progression of the hepatocellular carcinoma (HCC). |
24531795 |
LncRNADisease
|
tongue squamous cell carcinoma |
qPCR etc. |
tongue cancer tissue |
up-regulated |
expression |
In our study, results indicated that lncRNA HOTTIP was highly expressed in TSCC compared with adjacent non-malignant tissues and positively correlated with T stage, clinical stage, and distant metastasis in TSCC patients. |
26058875 |
Lnc2Cancer
|
colorectal cancer |
qPCR etc. |
colorectal cancer samples and 21 adjacent non-malignant samples |
up-regulated |
expression |
Our results indicated that lncRNA HOTTIP was highly expressed in CRC compared with adjacent non-malignant tissues (P<0.001), and positively correlated with T stage (T1-2 vs. T3-4, P = 0.001), clinical stage (I-II stages vs. III-IV stages, P = 0.003), and distant metastasis (absent vs. present, P = 0.014) in CRC patients. Furthermore, we also observed that increased lncRNA HOTTIP expression was an unfavorable prognostic factor in CRC patients (P = 0.001), regardless of T stage, distant metastasis and clinical stage. Finally, overexpression of lncRNA HOTTIP was supposed to be an independent poor prognostic factor for CRC patients through multivariate analysis (P = 0.017). |
26617875 |
Lnc2Cancer
|
osteosarcoma |
qPCR, knockdown etc |
osteosarcomas tissues and matched adjacent non-tumor tissues, cell lines(MG-63, HOS) |
up-regulated |
expression |
We found that HOTTIP expression was up-regulated in OS tissues, and correlated with advanced clinical stage and distant metastasis. OS patients with high HOTTIP expression level had poorer overall survival than those with low HOTTIP expression. Multivariable Cox proportional hazards regression analysis suggested that increased HOTTIP expression was an independent prognostic factor of overall survival in OS patients. Moreover, the results of in vitro assays showed that the suppression of HOTTIP in OS cells significantly reduced cell proliferation, migration and invasion ability |
26617868 |
Lnc2Cancer
|
hepatocelluar carcinoma |
qPCR, Luciferase reporter assay etc. |
cell lines (BEL7402, MHCC97H, MHCC97H-Luc) |
up-regulated |
regulation |
In our profiling study, HOTTIP was identified as the most significantly up-regulated lncRNA in human HCCs, even in early stage of HCC formation. HOTTIP is a novel oncogenic lncRNA, which negatively regulated by miR-125b. Overexpression of HOTTIP contributes to hepatocarcinogenesis by regulating the expression of its neighboring protein-coding genes. |
25424744 |
Lnc2Cancer
|
hepatocelluar carcinoma |
qPCR, Western blot, knockdown etc. |
HCC tissue, cell lines (SNU182, SNU449, SNU423, SNU387, SNU475 etc.) |
up-regulated |
expression |
Long noncoding RNA HOTTIP/HOXA13 expression is associated with disease progression and predicts outcome in hepatocellular carcinoma patients. |
24114970 |
LncRNADisease Lnc2Cancer
|
colorectal cancer |
qPCR, Western blot, knockdown etc. |
CRC and adjacent non-tumor colorectal samples, cell lines (DLD-1, SW480, SW620, HCT116) |
up-regulated |
interaction |
We found that overexpression of HOTTIP is correlated with an advanced pathological stage and a larger tumor size. Moreover, functional analyses revealed that the knockdown of HOTTIP expression by small interfering RNA (siRNA) or small hairpin RNA (shRNA) could inhibit cell proliferation and induce cell apoptosis. More importantly, we observed that HOTTIP knockdown induced a marked increase in the number of cells in the G0/G1 phase and a reduction in the number of cells in the S phase in both DLD-1 cells and SW480 cells. An in vivo experiment also revealed that the knockdown of HOTTIP inhibited tumor growth. Western blot and immunohistochemistry analyses indicated that HOTTIP potentially contributed to CRC cell growth partially through the silencing of p21 expression. |
26678886 |
Lnc2Cancer
|
hirschsprung disease |
qRT-PCR, Small RNA interference |
colon tissues rom 79 patients with Hirschsprung disease (HSCR) |
down-regulated |
expression |
LncRNA HOTTIP and HOXA13 were significantly down-regulated in HSCR compared to the controls. Meanwhile, the declined extent of their expression levels makes sense between two main phenotype of HSCR. Our study demonstrates that aberrant reduction of HOTTIP and HOXA13, which have a bidirectional regulatory loop, may play an important role in the pathogenesis of HSCR. |
26043692 |
|
prostate cancer |
sciliencing or knockdown of HOTTIP |
prostate cancer tumorigenesis |
down-regulated |
N/A |
down-regulation of HOTTIP and HOXA13 was associated with cell growth and cell cycle. |
27064878 |
|
|