Non-coding RNA UCA1 Research Articles

Long noncoding RNA UCA1 inhibits epirubicin-induced apoptosis by activating PPARα-mediated lipid metabolism

Metabolic reprogramming is a hallmark of cancer, and abnormal lipid metabolism is associated with drug resistance in bladder cancer cells. The long noncoding RNA (lncRNA) UCA1 is overexpressed in bladder cancer, but its functional contribution to lipid metabolism remains uncharacterized. In this study, we demonstrated that lncRNA UCA1 inhibits epirubicin-induced cell apoptosis by supporting abnormal lipid metabolism in bladder cancer cells. Mechanistically, lncRNA UCA1 promotes lipid accumulation in vitro and in vivo by upregulating PPARα mRNA and protein expression, which is mediated by miR-30a-3p. Knockdown of lncRNA UCA1 increased epirubicin-induced apoptosis via miR-30a-3p/PPARα and downstream p-AKT/p-GSK-3β/β-catenin signaling. Furthermore, mixed free fatty acids upregulated lncRNA UCA1 expression by promoting recruitment of the transcription factor RXRα to the lncRNA UCA1 promoter. These findings were verified in a mouse xenograft model and are consistent with the expression patterns in human bladder cancer patients. Overall, these findings establish the role of lncRNA UCA1 in lipid metabolism and bladder cancer cell resistance to epirubicin, suggesting that lncRNA UCA1 may serve as a candidate target for enhancing bladder cancer chemotherapy.

Downregulated expression of exosomal long non-coding RNA UCA1 in plasma of patients with non-small cell lung cance

Long non-coding RNAs (lncRNAs), mainly found in the nucleus of cells, are involved in different gene expression and regulation processes. Growing evidence has shown that abnormalities in the expression levels of lncRNAs play an important role in tumour metastasis, invasion, and proliferation, especially in non-small cell lung cancer (NSCLC). LncRNAs were also found to be upregulated or downregulated in exosomes secreted by cancer cells, thus they have the potential to be used as a non-invasive cancer biomarker. In this study, the expression of exosomal lncRNA UCA1 was determined on 29 plasma samples of patients with NSCLC and 29 controls who did not have NSCLC or related lung diseases by quantitative PCR using SYBR Green. Then, statistical analyses were used to evaluate the association between the expression of lncRNA UCA1 and some pathological features of NSCLC. The results showed that lncRNA UCA1 was downregulated in the exosomes of NSCLC patients compared with the control group (p=0.050), especially in the early stage (stage I + II). However, there was no association between the expression of lncRNA UCA1 and some pathological features of NSCLC, such as age, sex, smoking, alcohol consumption, tumour size, disease stage, lymph nodes, or tumour metastasis. This study provided the initial data on the expression of exosomal lncRNA UCA1 in the plasma of Vietnamese patients with NSCLC and further studies on the larger samples are needed to be continued.

Long noncoding RNA UCA1 promotes the chondrogenic differentiation of human bone marrow mesenchymal stem cells via regulating PARP1 ubiquitination.

Bone marrow mesenchymal stem cells (BMSCs) possess the potential to differentiate into cartilage cells. Long noncoding RNA (lncRNAs) urothelial carcinoma associated 1 (UCA1) has been confirmed to improve the chondrogenic differentiation of marrow mesenchymal stem cells (MSCs). Herein, we further investigated the effects and underlying mechanisms of these processes. The expression of UCA1 was positively associated with chondrogenic differentiation and the knockdown of UCA1 has been shown to attenuate the expression of chondrogenic markers. RNA pull-down assay and RNA immunoprecipitation showed that UCA1 could directly bind to PARP1 protein. UCA1 could improve PARP1 protein via facilitating USP9X-mediated PARP1 deubiquitination. Then these processes stimulated the NF-κB signaling pathway. In addition, PARP1 was declined in UCA1 knockdown cells, and silencing of PARP1 could diminish the increasing effects of UCA1 on the chondrogenic differentiation from MSCs and signaling pathway activation. Collectively, these outcomes suggest that UCA1 could act as a mediator of PARP1 protein ubiquitination and develop the chondrogenic differentiation of MSCs.

Diagnostic value and cognitive regulatory roles of long non-coding RNA UCA1 in Alzheimer’s disease

BackgroundTo explore the diagnostic role and potential mechanism of serum lncRNA UCA1 in Alzheimer's disease (AD). MethodsUCA1 concentration was determined using quantitative RT-PCR. The receiver operating characteristic curve was plotted to assess the diagnostic value. Cell viability and apoptotic capacity were assessed by cell counting kit-8 (CCK-8) and flow cytometry. Water maze experiments were used to test cognitive function in mice. The target genes of UCA1 were identified with a dual luciferase reporter assay. Functional and pathway analysis of miR-342-3p target genes was determined using enrichment analysis. ResultsThe concentration of UCA1 was elevated in the AD group and represented a diagnostic possibility of AD. The silenced UCA1 reduced the roles of Aβ on viability and apoptosis of SH⁃SY5Y cells by sponging miR-342-3p. The impaired cognitive impairment was partly recovered by the knockdown of the UCA1/miR-342-3p axis. Potential targets of miR-342-3p were enriched in function and pathways related to AD progression. ConclusionThe UCA1/miR-342-3p axis contributed to the occurrence of AD by regulating cognitive ability.

Metformin Suppresses the Proliferation and Promotes the Apoptosis of Colon Cancer Cells Through Inhibiting the Expression of Long Noncoding RNA-UCA1 [Retraction

[This retracts the article DOI: 10.2147/OTT.S245091.].

Long Noncoding RNA UCA1 Targets miR-582-5p and Contributes to the Progression and Drug Resistance of Bladder Cancer Cells Through ATG7-Mediated Autophagy Inhibition [Retraction

[This retracts the article DOI: 10.2147/OTT.S183940.].

LncRNA UCA1 promotes keratinocyte-driven inflammation via suppressing METTL14 and activating the HIF-1α/NF-κB axis in psoriasis

Keratinocytes are closely associated with innate immunity and inflammatory responses, and are dysregulated during the development of psoriasis, but the underlying mechanisms are not yet fully understood. This work aims to reveal the effects of long non-coding RNA (lncRNA) UCA1 in psoriatic keratinocytes. UCA1 was identified as a psoriasis-related lncRNA that highly expressed in psoriatic lesions. The transcriptome and proteome data of keratinocyte cell line HaCaT showed that UCA1 could positively regulate inflammatory functions, such as response to cytokine. Furthermore, UCA1 silencing decreased inflammatory cytokine secretion and innate immunity gene expression in HaCaT, its culture supernatant also decreased the migration and tube formation ability of vascular endothelial cells (HUVECs). Mechanistically, UCA1 activated the NF-κB signaling pathway, which is regulated by HIF-1α and STAT3. We also observed a direct interaction between UCA1 and N6-methyladenosine (m6A) methyltransferase METTL14. Knocking down METTL14 counteracted the effects of UCA1 silencing, indicating that it can suppress inflammation. In addition, the levels of m6A-modified HIF-1α were decreased in psoriatic lesions, indicating that HIF-1α is a potential target of METTL14. Taken together, this work indicates that UCA1 positively regulates keratinocyte-driven inflammation and psoriasis development by binding to METTL14, and activating HIF-1α and NF-κB signaling pathway. Our findings provide new insights into the molecular mechanisms of keratinocyte-driven inflammation in psoriasis.

Long Noncoding RNA UCA1 Promotes the Proliferation, Invasion, and Migration of Nasopharyngeal Carcinoma Cells via Modulation of miR-145 [Retraction

[This retracts the article DOI: 10.2147/OTT.S182290.].

Long non-coding RNA UCA1 correlates with electrophysiological abnormalties in atrial fibrillation

Long non-coding RNA UCA1 correlates with electrophysiological abnormalties in atrial fibrillation

Retraction: Exosomal long non-coding RNA UCA1 functions as growth inhibitor in esophageal cancer.

Esophageal cancer is a highly lethal and broad-spreading malignant tumor worldwide. Exosome-carrying lncRNAs play an essential role in the pathogenesis of various cancers. The results revealed that the expression of UCA1 was decreased in esophageal cancer tissues and plasma exosomes. UCA1 was enriched in exosomes, and exosomal UCA1 was a promising biomarker for the diagnosis of esophageal cancer with 86.7% sensitivity and 70.2% specificity. Overexpression of UCA1 played anticancer roles in esophageal cancer cells through inhibiting cell proliferation, invasion and migration, and colony formation. Also, exosomal UCA1 was taken up by esophageal cancer cells and inhibited the progression of esophageal cancer in vitro and tumor growth in vivo. Furthermore, exosomal UCA1 could directly target miRNA-613 in esophageal cancer cells. The results suggested that exosomal UCA1 inhibits tumorigenesis and progression of esophageal cancer in vitro and in vivo, and might be a promising biomarker for esophageal cancer. In this study, we determined the expression of UCA1 in esophageal cancer tissues, plasma exosomes of patients with esophageal cancer. We determined the potential of exosomal UCA1 as a biomarker and its effect on the pathogenesis and progression of esophageal cancer in vitro and in vivo.

Long Non-coding RNA UCA1 Regulates SRPK1 Expression Through miR- 99b-3p in Ovarian Cancer.

Ovarian carcinoma (OC) is one of the most common malignancies of the female reproductive organs, with a low survival rate primarily due to the lack of effective methods for early diagnosis and prognosis. In this article, our motivation is to explore the lncRNA-related network mechanisms involved in the pathogenesis of OC. Public lncRNAs and mRNA expression datasets for OC were collected from the Gene Expression Omnibus (GEO) database. By integrated bioinformatics analysis, we constructed a UCA1-miRNA-mRNA network. We studied lncRNA-related molecular modulation mechanism in ovarian cancer cells based on MTT assay, dual luciferase reporter gene assays, quantitative realtime PCR, and western blotting. UCA1 was higher in ovarian tumor tissues and cells than normal tissues and cells. It was demonstrated in this study that knockdown of UCA1 inhibited ovarian cancer cell viability, which a miR-99b-3p inhibitor could reverse in vitro. Further, UCA1 was shown to regulate the expression of SRPK1 by directly binding to miR-99b-3p. These results suggest that UCA1 functions as an oncogene in ovarian cancer. Inhibition of UCA1/miR-99b-3p/SRPK1 axis may become a novel target for treating ovarian cancer.

Analysis of Long Non-Coding RNA (lncRNA) UCA1, MALAT1, TC0101441, and H19 Expression in Endometriosis.

Endometriosis is a disease of complex etiology. Hormonal, immunological, and environmental factors are involved in its formation. In recent years, special attention has been paid to genetic mechanisms that can have a significant impact on the increased incidence of endometriosis. The study aimed to analyze the expression of four long non-coding RNA (lncRNA) genes, UCA1, MALAT1, TC0101441, and H19, in the context of the risk of developing endometriosis. The material for genetic testing for the expression of lncRNA genes were tissue slices embedded in paraffin blocks from patients with endometriosis (n = 100) and the control group (n = 100). Gene expression was determined by the RT-PCR technique. The expression of the H19 gene in endometriosis patients was statistically significantly lower than in the control group. A statistically significant association was found between H19 gene expression in relation to The Revised American Society for Reproductive Medicine classification of endometriosis (rASRM) in the group of patients with endometriosis. Research suggests that H19 expression plays an important role in the pathogenesis of endometriosis.

19 - The utility of non-coding RNA UCA1 as a urinary marker for bladder cancer

19 - The utility of non-coding RNA UCA1 as a urinary marker for bladder cancer

Knockdown of UCA1 attenuated the progression of alcoholic fatty disease by sponging miR-214.

Alcoholic fatty liver (AFL) is the initial manifestation of Alcoholic liver disease which can develop into alcoholic cirrhosis even extensive necrosis of liver cells, which induces liver failure finally. This study aims to focus on the role of long noncoding RNA UCA1 in AFL and further explored possible mechanism of this disease. We first downloaded GSE28619 to identify the expression of UCA1 in patients with AFL and use lncRNAs microarray to confirm UCA1 expression in serum of patients with AFL. Then we established ethanol-induced L02 cell model to mimic hepatocyte injury condition. By conducting qRT-PCR, we measured the expression of LncRNA UCA1 and miR-214 in serum of patients and ethanol-induced L02 cell. MTT assay, transwell migration, ELISA, qRT-PCR, and western blotting analysis were applied to evaluating the effect of UCA1 on ethanol-induced L02 cell. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. In this study, we first detected the expression of UCA1 was up-regulated in serum of patients with AFL and ethanol-induced L02 cells. And knockdown of UCA1 reversed the inhibiting effect of ethanol on the biological behavior of L02 cells including cell proliferation, migration, and apoptosis. Besides, lncRNA UCA1 regulated the expression of KLF5 by sponging miR-214. LncRNA UCA1 regulated the biological behavior of ethanol-induced L02 cells by sponging miR-214, which may provide novel therapeutic strategies for alcoholic fatty liver.

Long Non-Coding RNA UCA1 Correlates With Electropathology in Patients With Atrial Fibrillation

Long Non-Coding RNA UCA1 Correlates With Electropathology in Patients With Atrial Fibrillation

Long Noncoding RNA UCA1 Accelerates Nasopharyngeal Carcinoma Cell Progression by Modulating miR-124-3p/ITGB1 Axis [Retraction

[This retracts the article DOI: 10.2147/OTT.S215819.].

HES5 Activates Long Noncoding RNA UCA1 to Induce Colorectal Cancer Progression by Modulating miR-185/NOTCH3 Signaling.

Colorectal cancer (CRC) is one of the most common diagnosed cancers around the world. The poor prognosis and high fatality caused by metastasis are still the challenges for clinical treatment. Therefore, it is promising to clarify the detailed molecular mechanism of CRC metastasis. Accumulating evidences indicate that long noncoding RNAs (lncRNAs) play important roles in cancer progression including CRC. In this study, the function of lncRNA UCA1 was investigated. UCA1 was confirmed to be highly expressed in colorectal cancer. Moreover, the UCA1 expression level was positively related to tumor stages. Silencing UCA1 showed inhibitory effect on cell proliferation and metastasis. Both UCA1 and NOTCH3 were validated as direct targets of miR-185. Silencing UCA1 repressed NOTCH3 expression through the miR-185 sponge. NOTCH3 was found to be highly expressed in CRC patients and positively related to UCA1 expression. Furthermore, HES5 was verified as a transcription factor of UCA1, which induced UCA1 expression. In conclusion, UCA1 is a direct target of HES5. UCA1 promotes CRC metastasis through regulating the miR-185/NOTCH3 axis.

Retraction notice to "Long non-coding RNA UCA1 targets miR-185-5p and regulates cell mobility by affecting epithelial-mesenchymal transition in melanoma via Wnt/β-catenin signaling pathway" [Gene 676 (2018) 298-305

Retraction notice to "Long non-coding RNA UCA1 targets miR-185-5p and regulates cell mobility by affecting epithelial-mesenchymal transition in melanoma via Wnt/β-catenin signaling pathway" [Gene 676 (2018) 298-305

The Functional Role of Long Non-coding RNA UCA1 in Human Multiple Cancers: a Review Study

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LncRNA UCA1 stimulates the repair of hyperglycemic vascular smooth muscle cells through targeting miR-582-5p.

The purpose of this study was to elucidate the role of long non-coding RNA (lncRNA) UCA1 in inducing the repair of hyperglycemic vascular smooth muscle cells (VSMCs) by targeting microRNA-582-5p (miR-582-5p), thus alleviating diabetic angiopathy. Arterial vessels and serum exosomes were collected from 40 type 2 diabetes mellitus (T2DM) patients and 40 non-T2DM patients. Relative levels of UCA1 and miR-582-5p in collected samples were detected. Then, the interaction between UCA1 and miR-582-5p was assessed by Dual-Luciferase reporter assay. Moreover, the regulatory effects of UCA1 and miR-582-5p on VSMCs phenotypes were determined. Results showed that compared with non-T2DM patients, UCA1 was markedly downregulated, while miR-582-5p was upregulated in VSMCs and serum exosomes of T2DM patients. They exerted a negative expression correlation between each other. Besides, miR-582-5p was the direct target of UCA1. Under the induction of increased doses of glucose, UCA1 stimulated proliferative and invasive abilities in VSMCs. MiR-582-5p was responsible for the repairability of UCA1 in VSMCs under the hyperglycemia state. LncRNA UCA1 induces the repair of hyperglycemic VSMCs via negatively regulating miR-582-5p. UCA1 may be a novel target for T2DM diagnosis and treatment.