Table 1. A summary of lncRNAs involved in colorectal cancer development and progression.

LncRNA	In colorectal cancer, its expressions is:	Functions	Reference
Colon Cancer Associated Transcript 1 (CCAT1)	Upregulated	Promotes cellular proliferation, migration, and invasion.	[6]
Plasmacytoma variant translocation 1(PVT-1)	Upregulated	Promotes proliferation and invasion. Knockdown of PVT-1 promotes apoptosis in colorectal cancer cell lines by activating the TGF-β signaling pathway.	[7]
Colorectal Neoplasia Differentially Expressed (CRNDE)	Upregulated	Promotes colon cancer cell proliferation.	[8, 9, 10]
Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1)	Upregulated	Promotes cellular proliferation, migration, and invasion via 1) binding to SFPQ and releasing oncogene PTBP2 from SFPQ/PTBP2 complex 2) increasing expression of AKAP-9 via promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells.	[11, 12, 13]
ZNFX1 antisense RNA 1 (ZFAS1)	Upregulated	Silencing of ZFAS1 decreases CRC cell proliferation via G1-arrest of the cell cycle and decreasing CRC tumorigenicity. ZFAS1 acts as an oncogene in CRC via 1) destabilization of p53; 2) interaction with CDK1/cyclin B1 complex leading to cell cycle progression and suppression of apoptosis.	[14, 15, 16, 17]
MYC-induced lncRNAs (MYCLo-1, MYCLo-2, MYCLo-3)	Upregulated	Promotes MYC-modulated cell proliferation. MYCLo-1/−2 promote G1/S transition. MYCLo-3 decreases cellular time spent in the S and G2 phases.	[18]
MYC-repressed lncRNAs (MYCLo-4, MYCLo-5, MYCLo-6)	Downregulated	Inhibits MYC-enhanced cell proliferation. MYCLo-4/−6 increase G2 arrest. MYCLo-5 decreases cellular populations in the S phase.	[19]
Antisense noncoding RNA in the INK4 locus (ANRIL)	Upregulated	Promotes proliferation in a p15/p16-pRB pathway-independent manner, and promotes cell invasion and migration.	[20, 61]
urothelial carcinoma-associated 1 (UCA1)	Upregulated	Activates proliferation, suppresses apoptosis and cell cycle progression of CRC cells. UCA1 induces CRC migration and invasion and predicts poor prognosis.	[21, 22, 23]
BRAF-activated lncRNA (BANCR)	Downregulated	Inhibits the proliferation in part through upregulation of p21, induces the epithelial-mesenchymal transition (EMT) through an MEK/extracellular signal-regulated kinase-dependent mechanism.	[24, 33]
Maternally expressed gene 3 (MEG3)	Downregulated	Inhibits CRC cell proliferation and is an independent predictor for overall survival.	[25]
LncRNA loc285194	Downregulated	Suppresses tumor cell growth due to specific suppression of miR-211. Low expression of LOC285194 is associated with larger tumor size, higher tumor stage, more distant metastasis and poorer disease free survival.	[26, 27, 28]
Loc554202	Downregulated	Suppresses the cell proliferation, induces apoptosis, partly through activating specific caspase cleavage cascades, and inhibits CRC tumorigenesis.	[32]
LncRNA H19	Upregulated	Promotes EMT in CRC.	[34]
Hox transcript antisense intergenic RNA (HOTAIR)	Upregulated	Indicates poorer prognosis, promotes migration and invasion, enhances CSC properties, promotes cellular proliferation, decreases the expression of E-cadherin and increases expression of vimentin and MMP9.	[36, 49]
HOTTIP(‘HOXA transcript at the distal tip’ )	Upregulated	Predicts unfavorable prognosis for CRC patients.	[37]
Taurine up-regulated gene 1 (TUG1)	Upregulated	Increases the invasive and metastatic ability of CRC cells through activating EMT process and TUG1 overexpression indicates poor survival rates and a higher risk for cancer metastasis.	[38]
FEZF1 antisense RNA1 (FEZF1-AS1)	Upregulated	Promotes migration and proliferation through activating the G1-S checkpoint	[39]
Cancer susceptibility candidate 11 (CASC11)	Upregulated	Promotes CRC cell proliferation and metastasis by activation of WNT/β-catenin signaling.	[40]
91H	Upregulated	Promotes the proliferation, migration, and invasiveness of CRC cells.	[41]
LncRNA-CTD903	Downregulated	Predicts favorable prognosis in CRC patients and suppresses invasion and migration through repressing Wnt/β-catenin signaling.	[42]
LncRNA TINCR	Downregulated	Suppresses CRC proliferation and metastasis by accelerating the cleavage of EpCAM and releases EpICD via activating WNT/β- catenin pathway.	[43]
ncRAN	Downregulated	Inhibits in vitro migration and invasion of CRC cells and predicts CRC patient outcome.	[44]
Colon cancer-associated transcript 2 (CCAT2)	Upregulated	Promotes tumor growth, metastasis, and chromosomal instability. It functions as a WNT downstream target.	[46]
LncRNA-HIF2PUT	Upregulated	Promotes the HIF-2α expression and the CSC properties.	[48]
Lnc34a(locus mainly in the nucleus)	Upregulated	Enhances CSC self-renewal and tumorigenesis and suppresses miR-34a expression.	[50]
LincRNA-p21	Downregulated	Attenuates the viability, self-renewal, and glycolysis of CSCs.	[51]
LncRNA DANCR	Upregulated	Serves as a potential prognosis predictor for CRC prognosis, associates with TNM stage, histologic grade, and lymph node metastasis, and predicts shorter overall survival and disease-free survival time.	[52]
LncRNA FTX	Upregulated	Serves as an independent prognostic factor for CRC patients and is associated with differentiation grade, lymph vascular invasion, and clinical stage; indicates poorer overall survival.	[53]
Prostate cancer associated transcript 1(PCAT-1)	Upregulated	Functions as an independent prognostic factor for CRC patient outcome and implicates poorer overall survival.	[54, 55]
RP11-462C24.1	Downregulated	Serves as a prognosis indicator for CRC patients. Its down-regulation indicates increased distant metastasis and a poor disease-free survival.	[56]
PRNCR1	Upregulated	Serves as a sensitive diagnostic biomarker of CRC.	[57]
NEAT1	Upregulated	Functions as s diagnostic and prognostic biomarker of overall survival in CRC, associates with tumor differentiation, invasion, metastasis and TNM stage and predicts shorter disease-free survival time and overall survival time.	[58, 59]