| Related LncRNAs | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| ID | lncRNA Name | Disease | Method | Sample | Expression pattern | Dysfunction type | Description | PMID | Source |
| EL0556 | H19 | liver cancer | N/A | N/A | N/A | epigenetics | H19 ICR showed loss-of-imprinting in two steps and allelic histone marker signature during tumorigenesis showed similarity with ES cells. | 21163252 | LncRNADisease |
| EL0556 | H19 | liver cancer | N/A | N/A | N/A | regulation | Control of imprinting. Containing miRNA miR-675. | 22996375 | LncRNADisease |
| EL0556 | H19 | liver cancer | N/A | N/A | N/A | regulation | Control of imprinting breast, cervix, oesophagus prostate, endometrial, colon | 24499465 | LncRNADisease |
| EL0556 | H19 | liver cancer | qPCR etc. | hepatocellular carcinoma tissue | up-regulated | expression | LncRNA profiling revealed that CD90+ cells were enriched in lncRNA H19, and released this through exosomes.Experiments of gain and loss of function of H19 showed that this LncRNA plays an important role in the exosome-mediated phenotype of endothelial cells. Moreover, we suggest the lncRNA H19 as a putative therapeutic target in hepatocellular carcinoma. | 26272696 | Lnc2Cancer |
| EL0578 | HOTAIR | liver cancer | N/A | N/A | N/A | expression | In approximately one-quarter of human breast cancers, HOTAIR is highly induced, while its elevated levels are also predictive of metastasis and disease progression in other cancers, such as colon, colorectal, gastrointestinal, pancreatic and liver cancer. | 24667321 | LncRNADisease |
| EL0578 | HOTAIR | liver cancer | qPCR, Western blot, Luciferase reporter assay, RIP etc. | liver cancer tissue, cell line (hLCSC) | up-regulated | interaction | HOTAIR level was significantly higher in human hepatocarocinoma tissues and play tumorigenesis roles by downregulating SETD2 in liver cancer stem cells. HOTAIR may also mediate changes at an epigenetic level to affect gene expression and contribute to tumor aetiology. | 26172293 | Lnc2Cancer |
| EL0600 | HULC | liver cancer | N/A | N/A | N/A | expression | The highly upregulated lncRNA HULC in liver cancer was found in the blood of HCC patients, promising a potential biomarker. | 24531795 | LncRNADisease |
| EL0600 | HULC | liver cancer | N/A | N/A | N/A | N/A | PCGEM1, PCA3 (prostate cancer antigen 3, known also as DD3, differential display code 3) and PCNCR1 (prostate cancer ncRNA 4) are involved in prostate cancer, while HULC (highly up-regulated in liver cancer) is involved with liver cancer. | 24667321 | LncRNADisease |
| EL0600 | HULC | liver cancer | qPCR, Luciferase reporter assay, Western blot etc. | liver cancer tissue, cell lines (CREB, HULC, Prkacb etc.) | up-regulated | expression | Long non-coding RNA (lncRNA), highly up-regulated in liver cancer (HULC) plays an important role in tumorigenesis. Depletion of HULC resulted in a significant deregulation of several genes involved in liver cancer. Although up-regulation of HULC expression. | 20423907 | LncRNADisease Lnc2Cancer |
| EL0600 | HULC | liver cancer | qPCR, Western blot, knockdown, ChIP, Luciferase reporter assay etc. | HCC tissue, cell lines (HepG2, Huh7, HepG2.2.15 etc.) | up-regulated | interaction | Levels of HULC were positively correlated with levels of SPHK1 and its product, sphingosine-1-phosphate (S1P), in patients HCC samples. HULC increased SPHK1 in hepatoma cells. Mechanistically, HULC activated the promoter of SPHK1 in hepatoma cells through the transcription factor E2F1. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) further showed that E2F1 was capable of binding to the E2F1 element in the SPHK1 promoter. HULC increased the expression of E2F1 in hepatoma cells and levels of HULC were positively correlated with those of E2F1 in HCC tissues. Intriguingly, HULC sequestered miR-107, which targeted E2F1 mRNA 3'UTR, by complementary base pairing. Functionally, si-SPHK1 remarkably abolished the HULC-enhanced tumor angiogenesis in vitro and in vivo. Taken together, we conclude that HULC promotes tumor angiogenesis in liver cancer through miR-107/E2F1/SPHK1 signaling. | 26540633 | Lnc2Cancer |
| EL0608 | IGF2-AS | liver cancer | qPCR, Northern blot etc. | liver cancer tissue | up-regulated | expression | Loss of imprinting of IGF2 sense and antisense transcripts in Wilms' tumor. | 12702581 | LncRNADisease Lnc2Cancer |
| EL0744 | lincRNA-LALR1 | liver cancer | qPCR, RIP etc. | liver cancer tissue | up-regulated | regulation | LncRNA-LALR1 accelerates hepatocyte proliferation during liver regeneration by activating Wnt/尾-Catenin signaling | 23483581 | LncRNADisease Lnc2Cancer |
| EL0747 | LINC-ROR | liver cancer | RT-PCR, knockdown | N/A | up-regulated | interaction | linc-RoR is a hypoxia-responsive lncRNA that is functionally linked to hypoxia signaling in HCC through a miR-145-HIF-1α signaling module. | 24463816 | |
| EL0768 | lnc-DILC | liver cancer | real-time PCR; pull down assay and oligoribonucleotides or oligodeoxynucleotides treatment | N/A | down-regulated | interaction | Depletion of lnc-DILC markedly enhanced LCSC expansion and facilitated HCC initiation and progression, whereas ectopic expression of lnc-DILC dramatically inhibited LCSC expansion. Mechanistically, lnc-DILC inhibited the autocrine IL-6/STAT3 signaling. | 26812074 | |
| EL0853 | MALAT1 | liver cancer | microarray, qPCR, Western blot, Luciferase reporter assay, RIP etc. | liver cancer tissue, cell lines (HepG2, Bel-7402, SMMC-7721, HEK-293T etc.) | differential expression | regulation | Mutual inhibition between YAP and SRSF1 maintains long non-coding RNA, Malat1-induced tumourigenesis in liver cancer. | 24468535 | LncRNADisease Lnc2Cancer |
| EL0853 | MALAT1 | liver cancer | N/A | N/A | N/A | regulation | Sequesters SR splicing factors to regulate alternative splicing. | 22996375 | LncRNADisease |
| EL0882 | MIR7-3HG | liver cancer | microarray, qPCR etc. | liver cancer tissue, cell lines (Huh7, Bel7402, Bel7721, HepG2 etc.) | down-regulated | N/A | Compared with normal human hepatocytes and adjacent noncancerous tissues, uc002mbe.2 expression level was significantly lower in the HCC cell lines and liver cancer tissues. The TSA-induced uc002mbe.2 expression was positively correlated with the apoptotic effect of TSA in HCC cells. Therefore, TSA-induced apoptosis of HCC cells is uc002mbe.2 dependent and reduced expression of uc002mbe.2 may be associated with liver carcinogenesis. | 23643933 | Lnc2Cancer |
| EL0940 | MT1DP | liver cancer | qPCR, Western blot, Luciferase reporter assay etc. | cell lines (SMMC-7721, Bel-7402, Huh7, HepG2, DLD-1, LS174T) | down-regulated | interaction | Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effetc, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. | 25261601 | Lnc2Cancer |
| EL1416 | uc001lsz | liver cancer | qPCR etc. | cell lines (SMMC-7721, HepG2) | down-regulated | N/A | We found that comparing with respective normal cell line, uc001lsz was lowly expressed in gastric cancer (AGS, MGC-803 and SGC-7901), lung cancer (A549) and liver cancer (SMMC-7721 and HepG2) cell lines, while only highly expressed in prostate cancer (Du-145 and PC-3) cell lines (Figure 3C). | 24063685 | Lnc2Cancer |
| EL1431 | UCA1 | liver cancer | qPCR, Western blot, ISH, RIP, ChIP etc. | Human liver cancer stem cell line | up-regulated | interaction | Herein, we demonstrate excessive CUDR cooperates with excessive CyclinD1 or PTEN depletion to accelerate liver cancer stem cells growth and liver stem cell malignant transformation in vitro and in vivo. | 26513297 | Lnc2Cancer |
| EL1431 | UCA1 | liver cancer | qPCR, Western blot, RIP etc. | cells line (MEL-2) | up-regulated | interaction | Herein, we demonstrate that SET1A cooperates with CUDR to accelerate hepatocarcinogenesis and promote malignant transformation of hepatocyte-like stem cells. Mechanistically, CUDR enhances the phosphorylation of RB1, C-myc expression, and the interplay between the SET1A and pRB1. Notably, CUDR acts as a sponge cushion that shows a link between SET1A and pRB1, producing a activated pRB1-SET1A complex. | 26581161 | Lnc2Cancer |