Related LncRNAs |
ID |
lncRNA Name |
Disease |
Method |
Sample |
Expression pattern |
Dysfunction type |
Description |
PMID |
Source |
EL0090 |
ASK00420 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
down-regulated |
N/A |
LncRNA expression was then analyzed in CC cells and normal, primary cervical epithelial cells in the same manner. The levels of TI17313, TI13831, TI10124, and TI18318 were increased in 3 cancer cell lines (HeLa, SiHa, and CaSki) when compared with normal, primary cervical epithelial cells. Expression of the 5 other lncRNAs was below the level of detection in cultured cells. |
25007342 |
Lnc2Cancer
|
EL0237 |
BCYRN1 |
cervical cancer |
ISH, Northern hybridization etc. |
cervical cancer tissue |
up-regulated |
expression |
BC200 RNA was expressed in carcinomas of the breast, cervix, oesophagus, lung, ovary, parotid, and tongue, but not in corresponding normal tissues. |
9422992 |
LncRNADisease Lnc2Cancer
|
EL0278 |
CCAT2 |
cervical cancer |
quantitative real-time PCR |
cervical cancer cell lines |
up-regulated |
N/A |
CCAT2 knockdown inhibited cell proliferation in HeLa, CaSki and SiHa cells |
26983975 |
|
EL0283 |
CCEPR |
cervical cancer |
qPCR, Western blot, knockdown, RNA pull-down assay etc. |
cervical cancer tissue, cell lines (HeLa, SiHa) |
up-regulated |
interaction |
In this study, we found that cervical carcinoma high-expressed lncRNA 1 (lncRNA-CCHE1) was significantly upregulated in cervical cancer tissues. The higher expression of CCHE1 was significantly correlated with large tumor size, advanced Federation of Gynecology and Obstetrics stage, uterine corpus invasion, and poor survival. CCHE1 plays a pivotal role in cervical cancer cell proliferation via increasing PCNA expression and serves as a potential prognostic biomarker and therapeutic target in human cervical cancer. |
25921283 |
Lnc2Cancer
|
EL0285 |
CCND1 |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
up-regulated |
N/A |
Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR and MALAT1 was clearly evident in BLM-treated HeLa and MCF cells. For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. |
22487937 |
LncRNADisease Lnc2Cancer
|
EL0289 |
CDKN2B-AS1 |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
up-regulated |
expression |
Down-regulated in cells were incubated in the presence of BLM for 24 h or irradiated. |
22487937 |
LncRNADisease Lnc2Cancer
|
EL0289 |
CDKN2B-AS1 |
cervical cancer |
qPCR, knockdown etc. |
cell lines (HeLa) |
up-regulated |
interaction |
qRT-PCR showed that ANRIL is highly expressed in these cancer cells compared to normal fibroblasts. Depletion of ANRIL increased p15 expression, with no impact on p16 or ARF (alternative reading frame) expression, and caused cell-cycle arrest at the G2/M phase, leading to inhibition of proliferation of H1299 and HeLa cells. |
26408699 |
Lnc2Cancer
|
EL0526 |
GAS5 |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
up-regulated |
N/A |
Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR and MALAT1 was clearly evident in BLM-treated HeLa and MCF cells. For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. |
22487937 |
LncRNADisease Lnc2Cancer
|
EL0526 |
GAS5 |
cervical cancer |
qPCR, knockdown etc. |
cervical cancer tissue |
down-regulated |
expression |
We found that GAS5 expression was markedly downregulated in cervical cancer tissues than in corresponding adjacent normal tissues. Decreased GAS5 expression was significantly correlated with FIGO stage, vascular invasion and lymph node metastasis. Moreover, cervical cancer patients with GAS5 lower expression have shown significantly poorer overall survival than those with higher GAS5 expression. And GAS5 expression was an independent prognostic marker of overall survival in a multivariate analysis. |
25400758 |
Lnc2Cancer
|
EL0556 |
H19 |
cervical cancer |
N/A |
N/A |
N/A |
mutation |
High incidence of loss of heterozygosity and abnormal imprinting of H19 and IGF2 genes in invasive cervical carcinomas. |
8570220 |
LncRNADisease
|
EL0578 |
HOTAIR |
cervical cancer |
microarray, qPCR, RIP etc. |
cervical cancer tissue, cell line (C33-A) |
down-regulated |
interaction |
We identified significant linear trend of progressive HOTAIR down-regulation through HPV negative controls, HPV16 positive non-malignants and CaCx samples. Majority of CaCx cases portrayed HOTAIR down-regulation in comparison to HPV negative controls, with corresponding up-regulation of HOTAIR target, HOXD10, and enrichment of cancer related pathways. However, a small subset had significantly higher HOTAIR expression, concomitant with high E7 expression and enrichment of metastatic pathways. Expression of HOTAIR and PRC2-complex members (EZH2 and SUZ12), showed significant positive correlation with E7 expression in CaCx cases and E7 transfected C33A cell line, suggestive of interplay between E7 and HOTAIR. |
26152361 |
Lnc2Cancer
|
EL0578 |
HOTAIR |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
down-regulated |
N/A |
Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR and MALAT1 was clearly evident in BLM-treated HeLa and MCF cells. For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. |
22487937 |
LncRNADisease Lnc2Cancer
|
EL0578 |
HOTAIR |
cervical cancer |
qPCR etc. |
cervical cancer tissue |
up-regulated |
expression |
Overexpression of?long?noncoding?RNA?HOTAIR predicts a poor prognosis in patients with cervical cancer. |
24748337 |
LncRNADisease Lnc2Cancer
|
EL0578 |
HOTAIR |
cervical cancer |
qPCR etc. |
blood (serum) |
up-regulated |
expression |
Compared with normal control, the expression of HOTAIR was significantly upregulated in the sera of cervical cancer patients. In addition, elevated HOTAIR was associated with advanced tumor stages, adenocarcinoma, lymphatic vascular space invasion, and lymphatic node metastasis. In addition, our follow-up data showed that high HOTAIR was notably correlated with tumor recurrence and short overall survival. |
25366139 |
Lnc2Cancer
|
EL0578 |
HOTAIR |
cervical cancer |
qPCR, Western blot etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, C33A, CaSki) |
differential expression |
regulation |
Stable knockdown of HOTAIR significantly suppressed tumor growth and sensitized cervical cancer to radiotherapy in vivo. |
25547435 |
Lnc2Cancer
|
EL0578 |
HOTAIR |
cervical cancer |
qPCR, Western blot, knockdown etc. |
cervical cancer tissue, cell lines (SiHa, HeLa, Caski) |
up-regulated |
expression |
The expression level of HOTAIR in cervical cancer tissues was higher than that in corresponding non-cancerous tissues. High HOTAIR expression correlated with lymph node metastasis, and reduced overall survival. Moreover, HOTAIR regulated the expression of vascular endothelial growth factor, matrix metalloproteinase-9 and epithelial-to-mesenchymal transition (EMT)-related genes, which are important for cell motility and metastasis. |
25405331 |
Lnc2Cancer
|
EL0853 |
MALAT1 |
cervical cancer |
Microarray, knockdown, RT-PCR, western blot, and immunofluorescence |
cervical cancer (CC) cells and tissues |
up-regulated |
expression |
The down-regulation of MALAT1 by shRNA in CC cells inhibited the invasion and metastasis in vitro and in vivo. MALAT1 functions to promote cervical cancer invasion and metastasis via induction of EMT, and it may be a target for the prevention and therapy of cervical cancers. |
26798987 |
|
EL0853 |
MALAT1 |
cervical cancer |
N/A |
N/A |
N/A |
expression |
Overexpressed MALAT1 was found in many solid tumors such as lung cancer, cervical cancer, and HCC. |
24757675 |
LncRNADisease
|
EL0853 |
MALAT1 |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
up-regulated |
Interaction |
MALAT1 was involved in cervical cancer cell growth, cell cycle progression, and invasion through the regulation of gene expression, such as caspase-3, -8, Bax, Bcl-2, and BclxL. |
20213048 |
LncRNADisease Lnc2Cancer
|
EL0853 |
MALAT1 |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
down-regulated |
N/A |
Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR and MALAT1 was clearly evident in BLM-treated HeLa and MCF cells. For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. |
22487937 |
LncRNADisease Lnc2Cancer
|
EL0853 |
MALAT1 |
cervical cancer |
qPCR etc. |
cervical cancer tissue, cell lines (HeLa, CaSki, SiHa, HCC94 etc.) |
up-regulated |
N/A |
In the present study, it was identified that MALAT1 expression was upregulated in cervical cancer cell lines compared with normal cervical squamous cell samples. Further study into the effect of MALAT1 on cellular phenotype revealed that MALAT1 was able to promote cell migration and proliferation. HPV correlates with MALAT1 deregulation in cervical cancer. |
24932303 |
Lnc2Cancer
|
EL0853 |
MALAT1 |
cervical cancer |
qPCR, knockdown etc |
Tumor and adjacent normal tissues, cervical cancer cell lines(HeLa, CaSki) |
up-regulated |
expression |
MALAT1 expression is significantly increased in cervical cancer than in normal tissues. Its expression in the cancerous tissues is also significantly higher than in adjacent normal tissues. MALAT1 expression is correlated with tumor size, FIGO stage, vascular invasion and lymph nodes metastasis and is an independent predictor for overall survival of cervical cancer. When endogenous MALAT1 was knocked down, the cancer cells had significantly reduced proliferation and invasion and increased apoptosis |
26400521 |
Lnc2Cancer
|
EL0853 |
MALAT1 |
cervical cancer |
qPCR, Luciferase reporter assays, knockdown, RIP, RNA pull-down assay etc. |
cervical cancer tissue, cell lines (HeLa and CaSki) |
up-regulated |
interaction |
We found MALAT1 expression was significantly higher in radioresistant than in radiosensitive cancer cases. In addition, MALAT1 and miR-145 expression inversely changed in response to irradiation in HR-HPV+ cervical cancer cells. By using clonogenic assay and flow cytometry analysis of cell cycle distribution and apoptosis, we found CaSki and Hela cells with knockdown of MALAT1 had significantly lower colony formation, higher ratio of G2/M phase block and higher ratio of cell apoptosis. |
26311052 |
Lnc2Cancer
|
EL0853 |
MALAT1 |
cervical cancer |
qPCR, Northern blot, etc. |
cell line (HeLa) |
differential expression |
N/A |
We first examined the decay of MALAT-1 in various cancer cells (H1299, H1975, A549, HT1080, and HeLa TO cells) by DRB chase experiments using 7SK RNA as a control. Half-lives of MALAT-1 in H1299, H1975, A549, HT1080, and HeLa TO cells were > 12, 12, 12, 12, and 9 h, respectively. MALAT-1 stabilities varied in various cancer cells. |
22491206 |
Lnc2Cancer
|
EL0853 |
MALAT1 |
cervical cancer |
qPCR, Western blot, Luciferase reporter assay, knockdown, FCA etc. |
HR-HPV+ cervical cancer tisssue, cell lines (HeLa, CaSki, SiHa) |
up-regulated |
interaction |
Findings of this study confirmed higher MALAT1 expression in HR-HPV (+) cervical cancer. Knockdown of endogenous MALAT1 significantly reduced cell growth rate and invasion and increased cell apoptosis of Hela and siHa cells. Besides, knockdown of MALAT1 increased the expression of miRNA-124, while ectopic expression of miR-124 decreased MALAT1 expression. MALAT1 can indirectly modulate GRB2 expression via competing miR-124. Knockdown of GRB2 reduced cell invasion and increased cell apoptosis. In conclusion, MALAT1 can promote HR-HPV (+) cancer cell growth and invasion at least partially through the MALAT1-miR-124-RBG2 axis. |
26242259 |
Lnc2Cancer
|
EL0861 |
MEG3 |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
up-regulated |
N/A |
Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR and MALAT1 was clearly evident in BLM-treated HeLa and MCF cells. For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. |
22487937 |
LncRNADisease Lnc2Cancer
|
EL0861 |
MEG3 |
cervical cancer |
qPCR, ISH etc. |
cervical cancer tissue |
down-regulated |
N/A |
A pituitary-derived MEG3 isoform functions as a growth suppressor in tumor cells. |
14602737 |
LncRNADisease Lnc2Cancer
|
EL0861 |
MEG3 |
cervical cancer |
qPCR, Western blot, knockdown etc. |
cervical cancer, cell lines (HeLa, CaSki) |
down-regulated |
interaction |
We observed that MEG3 was downregulated in cervical cancer tissues, compared to the adjacent normal tissues, and was negatively related with FIGO stages, tumor size, lymphatic metastasis, HR-HPV infection and the expression of homo sapiens microRNA-21 (miR-21). Furthermore, we focused on the function and molecular mechanism of MEG3, finding that overexpression of MEG3 reduced the level of miR-21-5p expression, causing inhibition of proliferation and increased apoptosis in cervical cancer cells. In summary, our findings indicate that MEG3 function as a tumor suppressor by regulating miR-21-5p, resulting in the inhibition of tumor growth in cervical cancer. |
26574780 |
Lnc2Cancer
|
EL0861 |
MEG3 |
cervical cancer |
qPCR, Western bolt etc. |
cervical cancer tissue, cell lines (HeLa, C-33A, HCC94 etc.) |
down-regulated |
N/A |
qPCR results showed high expression levels of MEG3 in non-neoplastic tissues, but markedly lower levels in cancer tissues. Ectopic expression of MEG3 inhibited the proliferation of human cervical carcinoma cells HeLa and C-33A in vitro. On the other hand, knockdown of MEG3 promoted the growth of well-differentiated cervical carcinoma HCC94 cells. Further investigation into the mechanisms responsible for the growth inhibitory effects revealed that overexpression of MEG3 resulted in the induction of G2/M cell cycle arrest and apoptosis. |
23790166 |
Lnc2Cancer
|
EL1007 |
NPTN-IT1 |
cervical cancer |
qPCR etc. |
cervical cancer tissue |
down-regulated |
expression |
The results showed that lncRNA LET expression in cervical cancer tissues was significantly down-regulated compared with the adjacent non-tumor tissues (P < 0.05). Decreased lncRNA LET expression was significantly correlated with FIGO stage, lymph node metastasis, and depth of cervical invasion (P < 0.05), but not other clinical characteristics. |
25755778 |
Lnc2Cancer
|
EL1329 |
TI09485 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
down-regulated |
N/A |
LncRNA expression was then analyzed in CC cells and normal, primary cervical epithelial cells in the same manner. The levels of TI17313, TI13831, TI10124, and TI18318 were increased in 3 cancer cell lines (HeLa, SiHa, and CaSki) when compared with normal, primary cervical epithelial cells. Expression of the 5 other lncRNAs was below the level of detection in cultured cells. |
25007342 |
Lnc2Cancer
|
EL1330 |
TI10124 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
up-regulated |
N/A |
LncRNA expression was then analyzed in CC cells and normal, primary cervical epithelial cells in the same manner. The levels of TI17313, TI13831, TI10124, and TI18318 were increased in 3 cancer cell lines (HeLa, SiHa, and CaSki) when compared with normal, primary cervical epithelial cells. Expression of the 5 other lncRNAs was below the level of detection in cultured cells. |
25007342 |
Lnc2Cancer
|
EL1331 |
TI13831 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
up-regulated |
N/A |
LncRNA expression was then analyzed in CC cells and normal, primary cervical epithelial cells in the same manner. The levels of TI17313, TI13831, TI10124, and TI18318 were increased in 3 cancer cell lines (HeLa, SiHa, and CaSki) when compared with normal, primary cervical epithelial cells. Expression of the 5 other lncRNAs was below the level of detection in cultured cells. |
25007342 |
Lnc2Cancer
|
EL1332 |
TI18318 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
up-regulated |
N/A |
LncRNA expression was then analyzed in CC cells and normal, primary cervical epithelial cells in the same manner. The levels of TI17313, TI13831, TI10124, and TI18318 were increased in 3 cancer cell lines (HeLa, SiHa, and CaSki) when compared with normal, primary cervical epithelial cells. Expression of the 5 other lncRNAs was below the level of detection in cultured cells. |
25007342 |
Lnc2Cancer
|
EL1333 |
TI21327 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
down-regulated |
N/A |
LncRNA expression was then analyzed in CC cells and normal, primary cervical epithelial cells in the same manner. The levels of TI17313, TI13831, TI10124, and TI18318 were increased in 3 cancer cell lines (HeLa, SiHa, and CaSki) when compared with normal, primary cervical epithelial cells. Expression of the 5 other lncRNAs was below the level of detection in cultured cells. |
25007342 |
Lnc2Cancer
|
EL1334 |
TI22687 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
down-regulated |
N/A |
LncRNA expression was then analyzed in CC cells and normal, primary cervical epithelial cells in the same manner. The levels of TI17313, TI13831, TI10124, and TI18318 were increased in 3 cancer cell lines (HeLa, SiHa, and CaSki) when compared with normal, primary cervical epithelial cells. Expression of the 5 other lncRNAs was below the level of detection in cultured cells. |
25007342 |
Lnc2Cancer
|
EL1346 |
TMPOP2 |
cervical cancer |
microarray, qPCR, Western blot, knockdown, RIP etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, CaSki) |
up-regulated |
N/A |
lncRNA-EBIC was upregulated in cervical cancer. lncRNA-EBIC was an oncogenic lncRNA, which could promote tumor cell invasion in CC by binding to EZH2 and inhibiting E-cadherin expression. |
25007342 |
Lnc2Cancer
|
EL1349 |
TP53COR1 |
cervical cancer |
qPCR etc. |
cell line (CaSki) |
up-regulated |
N/A |
Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR and MALAT1 was clearly evident in BLM-treated HeLa and MCF cells. For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. |
22487937 |
LncRNADisease Lnc2Cancer
|
EL1403 |
TUSC8 |
cervical cancer |
qPCR, Western blot, knockdown etc. |
cervical cancer tissue, cell lines (HeLa, SiHa, HCC94) |
down-regulated |
expression |
Low expression of long noncoding XLOC_010588 indicates a poor prognosis and promotes proliferation through upregulation of c-Myc in cervical cancer. |
24667250 |
LncRNADisease Lnc2Cancer
|
|