Table 1.
LncRNA Name | Mode of Action | Associated Pathway | Cancer Context | Ref. |
---|---|---|---|---|
H19 | Translational control | Various | Enhances EMT and metastasis in various cancers | [23,24] |
PCA3 | Translational control | Androgen Receptor (AR) signaling | Prostate cancer biomarker | [25] |
HOTAIR | Control of chromatin-modifying complexes | Estrogen Receptor (ER) signaling | Increase invasiveness and metastasis, contribute to chemoresistance in breast cancer | [27,28] |
XIST | Spatial chromatin organization | XCI, miRNA regulation | Oncogene in multiple cancers | [29] |
GAS5 | Transcriptional control | Growth Receptor (GR) | Tumor suppressor | [30,31] |
TARID | Control of chromatin-modifying complexes | GADD45A-mediated DNA demethylation | Activation of tumor suppressor TCF21 | [32,33] |
Khps1 | Control of chromatin-modifying complexes | Cell cycle regulation, apoptosis, cell proliferation | Activation of proto-oncogene SPHK1 | [34] |
MEG3 | Control of chromatin-modifying complexes | TGF-β pathway | Associated with repressive chromatin in breast cancer cells | [35] |
lnc-LBCS | Control of chromatin-modifying complexes | Epigenetic silencing of SOX2 | Inhibit self-renewal and chemoresistance in bladder cancer stem cells | [36] |
NEAT-1 | Spatial chromatin organization | Transcription regulation, paraspeckle RNA retention | Overexpressed in human tumors and correlated with worse survival | [37,38,39,40] |
MALAT-1 | Spatial chromatin organization | Transcription regulation, EMT, apoptosis, autophagy | Aberrantly expressed in human cancers, as an oncogene (lung) or tumor repressor (glioma) | [41,42,43,44,45,46,47,48,49] |
MALAT-1 | Alternative splicing | Influence of splicing factor RSF1, SFPQ activity | Proto-oncogene in hepatocellular carcinoma, promotes tumor growth/metastasis in colorectal cancer | [50,51] |
NEAT-1 | Alternative splicing | Influence of splicing factor SFPQ activity | Overexpressed in human tumors and correlated with worse survival | [52,53,54] |
PNCTR | Alternative splicing | Pro-apoptotic splicing | Overexpressed in variety of cancer cells | [55] |
SAF | Alternative splicing | Pro-apoptotic signaling | Apoptotic resistance in human cancer cells | [56] |
NAT | Alternative splicing | Snail1-induced EMT | EMT in breast cancer cell lines | [57] |
TUG1 | miRNA sponging | VEGF-A axis | Increase angiogenesis in glioblastoma, contribute to hypervascularity in hepatoblastoma | [58,59] |
TUG1 | miRNA sponging | SOX2 and MYC expression | Upregulate abundance of stemness-associated TFs in glioma | [60] |
HOXA-AS2 | miRNA sponging | EGFR | Vasculogenic mimicry in glioma | [61] |
GAS5 | Translational control | c-Myc translation | Regulation of c-Myc in lymphoma cell lines | [62] |
treRNA | Translational control | E-cadherin translation | Upregulated in breast cancer primary and lymph-node metastasis | [63] |
NORAD | Protein stability | DNA damage, genomic stability | Often dysregulated in cancers | [64,65] |
SNHG15 | Protein stability | Slug signaling | Promotes colon cancer proliferation | [66] |
PSTAR | Protein stability | hnRNPK, p53 interaction and cell-cycle arrest | Tumor suppressor in hepatocelluilar carcinoma | [67] |
Note: Row color corresponds to “Mode of Action” as depicted in Figure 1.