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| Cancer type | Study subject | Cell line | Finding/mechanistic response | Reference |
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| Esophageal cancer | 90 ESCC patients who underwent surgery | EC109, EC9706, KYSE150, KYSE510, and NE1 | (i) LncRNA UCA1 was overexpressed and contributed to poor prognosis | [37] |
| (ii) Silenced lncRNA UCA1 decreased cell proliferation, migration, and invasion |
| 66 esophageal cancer patients underwent surgical resection | EC9706 and KYSE | (i) LncRNA UCA1 was overexpressed and contributed to poor prognosis | [38] |
| (ii) Sox4 was identified as a direct target gene of lncRNA UCA1 and acted as a ceRNA |
| (iii) LncRNA UCA1 reduced miR-204 level |
| 110 EC tissues and 60 paired of adjacent nontumorous tissues | EC1, EC109, EC9706, KYSE150, and Het-1A | (i) LncRNA UCA1 was overexpressed in EC tissues with advanced EC stages and was associated with poor prognosis | [39] |
| (ii) Overexpressed lncRNA UCA1 promoted cell proliferation and metastasis |
| (iii) LncRNA UCA1 promoted glycolysis by sequestering miR-203 to increase HK2 levels, resulting in enhanced Warburg effect |
| 106 newly diagnosed patients with primary cancer and previously untreated ESCC | EC109 | (i) LncRNA UCA1 lowly expressed in tumor tissue compared to the adjacent nontumor tissue | [40] |
| (ii) LncRNA UCA1 suppressed ESCC via inhibition of Wnt signaling pathway |
| (iii) LncRNA UCA1 reduced C-myc and active β-catenin protein expression |
| 15 paired EC tissues and adjacent normal tissues of EC patients | EC18, KYSE140, and NEEC | (i) LncRNA UCA1 expression was decreased in EC tissues and plasma exosomes | [41] |
| (ii) LncRNA UCA1 inhibited cell proliferation, invasion, migration, and colony formation as well as inhibited tumor growth in vivo |
| (iii) Exosomal lncRNA UCA1 directly targeted miRNA-613 in EC cells |
| Gastric cancer | 20 plasma samples of patients and pair-matched plasma samples | Five GC tissues and five pair-matched noncancerous tissues | (i) Overexpressed lncRNA UCA1 in both GC tissue and plasma of GC patients | [42] |
| (ii) Plasma lncRNA UCA1 provided higher diagnostic performance for the detection of GC |
| Gastric cancer | 112 patients diagnosed with GC | SGC-7901, BGC-823, MKN-28, AGS, and GES-1 | (i) Overexpressed lncRNA UCA1 in GC human tissue and GC cell lines | [43] |
| (ii) High lncRNA UCA1 expression correlated with worse differentiation, tumor size, invasion depth, and TNM stage |
| Chinese patients | BGC-823 and SGC-7901 | (i) Elevated lncRNA UCA1 in tumor tissues of GC patients | [44] |
| (ii) LncRNA UCA1 promoted metastasis by sponging miR-203, resulting in ZEB overexpression |
| Ten GC and ten paracancerous normal tissues from the patients in China | MGC‐803, SGC‐7901, BGC‐823, AGS, MKN‐45, and GES‐1. | (i) LncRNA UCA1 expression was higher in GC compared to paracancerous tissues | [45] |
| (ii) SATB1 and lncRNA UCA1 competitively bound to miR‐495‐3p that acts as a ceRNA and reduced its expression |
| 62 GC patients who underwent surgical resection | AGS, MKN-28, SGC-7901, MKN-45, and GES-1 | (i) Overexpressed lncRNA UCA1 in GC human tissue and GC cell lines | [46] |
| (ii) LncRNA UCA1 repressed miR-590-3p, leading to increased CREB1 expression |
| 40 primary GC tissues and corresponding adjacent nontumorous gastric tissue samples | AGS, SGC-7901, BGC-823, MGC-803, and SNU-1 | (i) Overexpressed lncRNA UCA1 in GC human tissue compared to adjacent noncancerous tissues | [47] |
| (ii) LncRNA UCA1 repressed miR-26a/b, miR-193a, and miR-214 expression through direct interaction |
| (iii) LncRNA UCA1 upregulated pdl1 |
| 37 paired GC tissues and corresponding adjacent normal tissues | HGC27, MGC803, NCI-N87, BGC-823, SGC7901, and GES-1 | (i) Overexpressed lncRNA UCA1 in GC human tissue compared to adjacent normal tissues | [48] |
| (ii) TGFb1-induced lncRNA UCA1 elevation and acceleration of EMT |
| 102 gastric cancer patients who underwent surgery | MKN-28, SGC-7901, MGC-803, BGC-823, MKN-45, and GES-1 | (i) The overexpression of UCA1 in GC was higher in GC tissue than adjacent noncancerous tissues, and it is correlated with TNM stage and lymph node metastases | [49] |
| (ii) LncRNA UCA1 activated PI3K-Akt-mTOR signaling pathway |
| 39 patients with GC | BGC-823, SGC-7901, AGS, MKN-45, NCI-N87, and MKN-28 | (i) LncRNA UCA1 highly expressed in GC tissues than its matched nontumor tissues | [50] |
| (ii) SP1 induced lncRNA UCA1 |
| (iii) EZH2 and lncRNA UCA1 interaction activated AKT/GSK-3B/cyclin D1 axis |
| 49 patients with GC | MGC-803, HGC-27, NCI-N87, and GES-1 | (i) LncRNA UCA1 was highly expressed in GC tissues than its adjacent nontumor tissues | [51] |
| (ii) LncRNA UCA1 promoted tumor metastasis by inducing GRK2 degradation, which activated the ERK-MMP9 signaling pathway |
| 28 primary GC patients who had not received previous chemotherapy or radiotherapy | SGC-7901, SGC-7901, SGC-7901/ADR, SGC-7901/DDP, and SGC-7901/FU | (i) LncRNA UCA1 was one of the lncRNAs overexpressed in GC tissue | [52] |
| (ii) Multidrug resistance of GC by repressing miR-27b |
| 53 pairs of GC tissues and adjacent normal tissues | GES-1, SNU-5, AGS, and NCI-N87 | (i) LncRNA UCA1 was highly expressed in GC tissues than its adjacent nontumor tissues | [53] |
| (ii) Knockdown of lncRNA UCA1 increased sensitivity to cisplatin by inducing cell apoptosis |
| (iii) LncRNA UCA1 reduced miR-513a-3p and elevated CYP1B1 |
| — | MGC-803 and BGC-823 | (i) LncRNA UCA1 promoted the migration of hypoxia-resistant GC cells via miR-7-5p/EGFR axis | [54] |
| Hepatobiliary cancer | 60 paired tumorous and adjacent nontumorous liver tissues obtained immediately after surgical resection | LO2 cells and HBx-expressing hepatoma cells | (i) HBx induced lncRNA UCA1 expression in hepatocytes | [55] |
| (ii) LncRNA UCA1 reduced p27kip1 expression and increased EZH2 expression via histone methylation on p27kip1 promoter region |
| (iii) LncRNA UCA1 induced CDK2 expression without altering CDK4 and CDK6 |
| 88 HCC patients | HepG2 and Huh7 | (i) LncRNA UCA1 highly expressed in 79 patients out of 88 HCC patients | [56] |
| (ii) TGF-β1 induced the expression of lncRNA UCA1 and HXK2 |
| 66 newly diagnosed HCC patients | SNU-398 and SNU-449 | (i) Overexpressed lncRNA UCA1 was detected in HCC tissues compared to healthy tissues | [57] |
| (ii) miR-124 repressed ROCK1 |
| (iii) ROCK1 reduced lncRNA UCA1 expression |
| (iv) HBV and HCV infections did not affect the expression of lncRNA UCA1 and miR-124 |
| 50 HCC patients from online data sets | HEK 293t and HepG2 | (i) Overexpressed SND1 in HCC tissues than normal tissues | [58] |
| (ii) SND1 induced lncRNA UCA1 expression through the interaction of SND1 with MYB |
| — | HepG2 | (i) Arsenic stress induced lncRNA UCA1 | [59] |
| (ii) LncRNA UCA1 promoted protective roles of arsenic-induced cell death by blocking autophagic flux |
| (iii) LncRNA UCA1 protected HCC cells against arsenic stress by repressing miR-184 and elevating OSGIN1 that activated mTOR/p70S6K autophagy inhibition pathway |
| 68 CCA patients | HCCC-9810, RBE, QBC939, Huh-28, HuCCT1, KMBC, CCLP-1, and HIBEC | (i) LncRNA UCA1 was overexpressed in CCA tissues and cell lines | [60] |
| (ii) LncRNA UCA1 inhibited apoptosis through Bcl-2/caspase-3 pathway |
| (iii) Activated AKT/GSK-3β axis elevated CCND1 expression |
| 22 CCA patients receiving surgical resection | LIPF155C, CCLP1, QBC939, huh28, and HIBEC | (i) LncRNA UCA1 was highly expressed lncRNA in CCA compared with paracarcinoma tissues | [61] |
| (ii) Regulation of miR-122/CLIC1 and activation of ERK/MAPK signaling pathway |
| 45 GBC tissues and neighboring noncancerous tissues from patients who underwent liver resection | NOZ and GBC-SD | (i) High expression of lncRNA UCA1 was associated with tumor size, lymph node metastasis, TNM stage, and short survival time in GBC patients | [62] |
| (ii) Recruitment of EZH2 to the promoter of p21 and E-cadherin |
| (iii) Epigenetically suppressed p21 and E-cadherin expression |
| Pancreatic cancer | 128 PC patients received operation as initial systemic treatment | Panc-1, Bxpc-3, Capan-1,SW-1990, and HPDE6C-7 | (i) LncRNA UCA1 overexpressed in PC tissue and cell lines | [63] |
| (ii) LncRNA UCA1 suppressed p27 protein |
| 50 PC patients | SW1990, BxPC-3, MiaPaCa-2, PANC-1, CAPAN-1, and HPDE | (iii) Highly expressed lncRNA UCA1 in PC tissues and cell lines | [64] |
| (iv) LncRNA UCA1 sponged miR135a |
| 36 PC patients underwent surgical resection | HPC-Y5, PANC-1, SW1990, and AsPC-1 | (i) Out of 19 lncRNAs, lncRNA UCA1 was one of the overexpressed lncRNAs in PC tissues | [65] |
| (ii) LncRNA UCA1 repressed miR-96, resulting in increased FOXO3 expression |
| Analysis of mRNA levels of lncRNA UCA1 in PC patients from BADEA and TCGA databases | BxPC-3, SW1990, PaTu8988, and PANC-1 | (i) Higher mRNA levels of lncRNA UCA1 in PC tissues than normal pancreatic tissues and correlated with poor prognosis | [66] |
| (ii) LncRNA UCA1 promoted cell migration and invasion via Hippo signaling pathway |
| Analysis of lncRNA UCA1 mRNA levels from TCGA database in PDAC tumor specimens and normal | PaTu8902, Mpanc96, HEK293T, and H6C7 | (i) LncRNA UCA1 was highly expressed in PDAC tumor specimens than normal tissue | [67] |
| (ii) LncRNA UCA1 acted as a ceRNA to increase the expression of KRAS via sponging miR-590-3p |
| (iii) KRAS promoted lncRNA UCA1 expression. |
| Colorectal cancer | 80 CRC patients | CaCO-2, SW480, HCT116, LoVo, and CCC-HIE-2 | (i) Overexpressed lncRNA UCA1 promoted cell proliferation, apoptosis, and cell cycle distribution | [68] |
| Two CRC cohorts, including 90 and 119 human primary CRC tissues and their paired adjacent noncancerous tissues, respectively | HEK-293T, HCT8, HCT116, HT29, LoVo, and SW480 | (i) Induced 5-FU resistance | [69] |
| (ii) Inhibition of miR-204-5p and upregulated its target genes (e.g., bcl2, rab22a, and creb1) |
| 60 CRC patients | NCM460, SW620, HT29, CACO2, SW480, and HCT116 | (i) Overexpressed lncRNA UCA1 in CRC tissues and cell lines | [70] |
| (ii) LncRNA UCA1 repressed miR‐28‐5p level, which subsequently increased HOXB3 axis |
| (iii) LncRNA UCA1 elevated MMP2 and MMP9 |
| — | CCD-18Co, HIEC-6, SW620, and HT29 | (i) Overexpressed lncRNA UCA1 in CRC cell lines | [71] |
| (ii) LncRNA UCA1 sponged miR-185-5p, leading to elevation of WNT1 and WISP2 that activated WISP2/b-catenin signaling pathway, which affected autophagy and survival of CRC |
| — | SW480, SW620, HT-29, CCD-18Co, and HIEC-6 | (i) Overexpressed lncRNA UCA1 in CRC cell lines | [72] |
| (ii) LncRNA UCA1 elevated the expression of MAPK14 to activate MAPKAPK2/HSP27 signaling pathway |
| — | SW480 and NF | (i) Overexpressed lncRNA UCA1 in CRC cell lines | [73] |
| (ii) CAFs induced lncRNA UCA1 to increase the expression of mTOR |
| (iii) LncRNA UCA1/mTOR axis repressed p27 and miR-143 and significantly elevated cyclin D1 and KRAS expression |
| Tissue from 32 CRC patients collected immediately after surgical resection | HCT116, CCL244, SW480, LoVo, and FHC | (i) LncRNA UCA1 significantly expressed higher in CRC tissue after chemoradiotherapy | [74] |
| (ii) Downregulation of LncRNA UCA1 enhanced radiotherapy sensitivity |
| (iii) LncRNA UCA1 inhibited EMT by reducing MMP2, MMP9, ZEB1, and vimentin |
| 25 CRC patients with 5-fluorouracil resistance and 25 CRC patients with 5-fluorouracil sensitivity | SW480, SW620, and 293T | (i) 5-fluorouracil resistance of CRC was associated with lncRNA UCA1 abundance that promoted autophagy and inhibited apoptosis | [75] |
| (ii) LncRNA UCA1 sponged miR-23b-3p and consequently elevated ZNF281 expression |
| 53 CRC patients treated with cetuximab | Caco2-CR and Caco2-CS | (i) LncRNA UCA1 levels upregulated in cetuximab-resistant cells and their exosomes | [76] |
| (ii) Exosomal lncRNA UCA1 was detectable and stable in the serum of CRC patients |
| (ii) Exosomes originated from cetuximab-resistant cells could alter lncRNA UCA1 expression |
| (iv) LncRNA UCA1 can be transferred from resistant cells to sensitive cells through exosomes |
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