Expression Levels Of Urothelial Carcinoma Associated 1 Research Articles

Effects of lncRNA-UCA1 targeting miR-204-5p on the proliferation, migration, apoptosis and immune escape of endometrial carcinoma cells

Objective: To investigate the effect of long non-coding RNA urothelial carcinoma-associated 1 (UCA1) gene on the proliferation, migration, apoptosis and immune escape of endometrial cancer cells and its molecular mechanism. Methods: Endometrial cancer tissues and adjacent normal tissues of patients with endometrioid adenocarcinoma who underwent total or partial hysterectomy in Henan Provincial People's Hospital from 2017 to 2019 were collected. The expressions of UCA1 and miR-204-5p were detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), and the cell proliferation, migration and apoptosis were detected by cell counting kit 8 (CCK8) method, Transwell method, flow cytometry, and dual-luciferase reporter assay was used to explore the target relationship between UCA1 and miR-204-5p. HEC-1A-sh-NC or HEC-1A-sh-UCA1 cells were co-cultured with peripheral blood mononuclear cells (PBMC) or cytokine-induced killer cells in vitro to explore the role of UCA1 in immune escape. Results: The expression level of UCA1 in endometrial cancer tissue (17.08±0.84) was higher than that in adjacent normal endometrial tissue (3.00±0.37), and the expression level of miR-204-5p (0.98±0.16) was lower than that in adjacent normal endometrial tissue (2.00±0.20, P<0.05). Pearson correlation analysis showed that the expression of miR-204-5p was negatively correlated with the expression of UCA1 (r=-0.330, P=0.030). The expressions of UCA1 and miR-204-5p were associated with the International Federation of Gynecology and Obstetrics stage of endometrial cancer, lymph node metastasis and vascular invasion (P<0.05). The relative ratio of absorbance (0.58±0.11) and the number of cell migration [(199.68±18.44)] in the sh-UCA1 group were lower than those in the sh-NC group (1.24±0.17 and 374.76±24.83), respectively. The apoptosis rate of sh-UCA1 group [(28.64±7.80)%] was higher than that of sh-NC group [(14.27±4.38)%, P<0.05]. After different ratios of effector cells and target cells were cultured, the cell survival rate of HEC-1A-sh-UCA1 group was lower than that of HEC-1A-sh-NC group, and the difference was statistically significant (P<0.05). UCA1 had a binding site for miR-204-5p. The relative ratio of absorbance (1.74±0.08) and the number of cell migration (426.00±18.00) cells in the UCA1+ anti-miR-204-5p group were higher than those in the control group [1.00±0.03 and (284.00±8.00) cells, respectively]. The apoptosis rate of UCA1+ anti-miR-204-5p group [(5.42±0.93)%] was lower than that of control group [(14.82±1.48)%, P<0.05]. HEC-1A-sh-UCA1 cells could induce higher interferon gamma (IFN-γ) expression when co-cultured with PBMC, and the levels of IFN-γ expression in PHA group and PHA+ pre-miR-204-5p group cells were 2.42±0.49 and 1.88±0.26, which were higher than that in the PHA+ pre-NC group (0.85±0.10, P<0.05). When co-cultured with cytokine-induced killer cells (different ratios) in vitro, the HEC-1A-sh-UCA1 group and the HEC-1A-pre-miR-204-5p group had lower survival rates than that in the HEC-1A-pre-miR-204-5p group. In the HEC-1A-pre-NC group, the differences were statistically significant (P<0.05). Conclusion: UCA1/miR-204-5p may play an important role in human endometrial cancer.

Long non-coding RNA UCA1 regulates MPP+-induced neuronal damage through the miR-671-5p/KPNA4 pathway in SK-N-SH cells.

Parkinson's disease (PD) is an age-related neurodegenerative disease. Long non-coding RNA urothelial carcinoma-associated 1 (UCA1) is involved in the pathogenesis of PD. However, the pathogenesis of PD regulated by UCA1 has not been fully explained. We used 1-Methyl-4-phenylpyridinium (MPP+)-induced SK-N-SH cells for functional analysis. Expression levels of UCA1, microRNA (miR)-671-5p, and KPNA4 (karyopherin subunit alpha 4) mRNA were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were analyzed using MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) or flow cytometry assays. Some protein levels were measured by western blotting. The levels of pro-inflammatory cytokines were tested by ELISA (enzyme-linked immunosorbent assay). The levels of LDH (lactate dehydrogenase), MDA (malondialdehyde), and SOD (superoxide dismutase) were measured using corresponding kits. The relationship between UCA1 or KPNA4 and miR-671-5p was verified by dual-luciferase reporter assay and/or RNA immunoprecipitation (RIP) assay. MPP+ induced UCA1 expression in SK-N-SH cells in a concentration-dependent manner or time-dependent manner. UCA1 knockdown reduced MPP+-induced apoptosis, inflammation, and oxidative stress in SK-N-SH cells. MiR-671-5p was downregulated while KPNA4 was upregulated in MPP+-treated SK-N-SH cells. UCA1 sponged miR-671-5p to regulate KPNA4 expression. MiR-671-5p inhibition counteracted UCA1 knockdown-mediated influence on apoptosis, inflammation, and oxidative stress of MPP+-induced SK-N-SH cells. KPNA4 overexpression offset the inhibitory influence of miR-671-5p mimic on apoptosis, inflammation, and oxidative stress of MPP+-treated SK-N-SH cells. UCA1 inhibition reduced MPP+-induced neuronal damage through the miR-671-5p/KPNA4 pathway in SK-N-SH cells, providing a novel mechanism to understand the pathogenesis of PD.

Knockdown of Long Noncoding RNA Urothelial Carcinoma-Associated 1 Represses Gallbladder Cancer Advancement by Regulating SPOCK1 Expression Through Sponging miR-613.

Background: Gallbladder cancer (GBC) is the most common biliary tract malignancy. Long noncoding RNA urothelial carcinoma-associated 1 (UCA1) and MicroRNA-613 (miR-613) have been reported to be involved in the progression of various cancers. However, the regulatory mechanism between UCA1 and miR-613 in GBC is unclear. Materials and Methods: The expression levels of UCA1, miR-613, and secreted protein/osteonectin, cwcv, and kazal-like domains proteoglycan 1 (SPOCK1) mRNA were detected using quantitative real-time polymerase chain reaction. Cell proliferation, migration, invasion, and apoptosis were determined with MTT, transwell, or flow cytometry assays. The levels of SPOCK1 protein, Bax, cleaved-casp-3, and Bcl-2 were determined by Western blot analysis. The relationship between miR-613 and UCA1 or SPOCK1 was verified through dual-luciferase reporter and/or RNA immunoprecipitation assays. Xenograft assay was performed to verify the role of UCA1 in vivo. Results: UCA1 and SPOCK1 were upregulated, whereas miR-613 was downregulated in GBC tissues and cells. UCA1 silencing decreased tumor growth in vivo and impeded proliferation, migration, invasion, and induced apoptosis of GBC cells in vitro. Notably, UCA1 acted as a sponge for miR-613, which targeted SPOCK1 in GBC cells. Moreover, UCA1 enhancement reversed the repressive impact of miR-613 mimic on the malignancy of GBC cells. UCA1 regulated SPOCK1 expression through adsorbing miR-613. Furthermore, SPOCK1 elevation overturned UCA1 silencing mediated the malignant behaviors of GBC cells. Conclusion: UCA1 knockdown suppressed GBC progression through downregulating SPOCK1 via sponging miR-613, providing an evidence for UCA1 as a target for GBC treatment.

The long non-coding RNA, urothelial carcinoma associated 1, promotes cell growth, invasion, migration, and chemo-resistance in glioma through Wnt/β-catenin signaling pathway.

The long non-coding RNA, urothelial carcinoma associated 1 (UCA1) has been demonstrated to play important roles in various types of cancers. This study investigated the functional role of UCA1 in glioma and explored the underlying molecular mechanisms. UCA1 was found to be highly up-regulated in glioma cells, and knock-down of UCA1 inhibited cell growth, invasion and migration, and also induced apoptosis in glioma cells. On the other hand, overexpression of UCA1 promoted cell proliferation, cell invasion and migration in glioma cells. Knock-down of UCA1 suppressed the activity of Wnt/β-catenin signaling, and treatment with lithium chloride restored the inhibitory effect of UCA1 knock-down on cell invasion and migration. More importantly, the aberrant expression of UCA1 was associated with chemo-resistance to cisplatin and temozolomide in glioma cells via interacting with Wnt/β-catenin signaling. In vivo studies showed that overexpression of UCA1 promoted the in vivo tumor growth of U87 cells in the nude mice. Clinically, UCA1 was found to be up-regulated in glioma tissues and higher expression level of UCA1 was correlated with poor survival in patients with glioma. Taken together, our results showed that UCA1 had a functional role in the regulation of glioma cell growth, invasion and migration, and chemo-resistance possibly via Wnt/β-catenin signaling pathway.

Long Noncoding RNA UCA1 Accelerates Nasopharyngeal Carcinoma Cell Progression By Modulating miR-124-3p/ITGB1 Axis.

BackgroundNasopharyngeal carcinoma (NPC) is a common malignant cancer that is distributed particularly in Southeastern Asia. Previous studies have manifested that long noncoding RNA urothelial carcinoma associated 1 (UCA1) was involved in NPC tumorigenesis and metastasis. However, the biological mechanism of UCA1 for NPC cell progression requires further investigation.MethodsThe expression levels of UCA1, miR-124-3p, integrin beta-1 (ITGB1) were detected by qRT-PCR. Protein expression of ITGB1 was determined by Western blot assay. Cell proliferation, migration and invasion were evaluated by CCK8 and transwell assay, respectively. The interaction between miR-124-3p and UCA1 or ITGB1 was determined by luciferase reporter system, RIP and RNA pull-down assay. Mice model was established by subcutaneously injecting SUNE1 cells stably transfected with sh-UCA1 and sh-NC.ResultsThe expression of UCA1 was up-regulated in NPC tissues and cells. However, UCA1 knockdown hindered NPC cell growth, migration and invasion. In addition, the interaction between miR-124-3p and UCA1 or ITGB1 was confirmed by luciferase reporter system, RIP and RNA pull-down assay. Besides, miR-124-3p inhibitor abrogated UCA1 silencing-mediated suppression on cell progression in NPC. Moreover, UCA1 accelerated NPC cell progression through modulating ITGB1 via sponging miR-124-3p. In vivo experiments revealed the interference of UCA1-inhibited tumor growth by regulating miR-124-3p/ITGB1 axis.ConclusionUCA1 acts as an oncogene to promote NPC cell proliferation by up-regulating ITGB1 through suppressing miR-124-3p in vitro and in vivo, providing a potential target for NPC diagnosis and treatment.

Function of Long Noncoding RNA UCA1 on Gastric Cancer Cells and its Clinicopathological Significance in Plasma.

Diagnosis and treatment of gastric cancer (GC) at early stages is challenging, causing great difficulties to patients. Long noncoding RNAs (lncRNAs) may serve both as novel molecular markers and therapeutic targets in diagnosis and prognosis of cancers. This study aimed to investigate the function of long non-coding RNA Urothelial Carcinoma Associated 1 (UCA1) on GC cells and evaluate its diagnostic value in GC. In total, 90 patients with GC and 43 healthy individuals were recruited for the study. Venous blood samples from 40 of the 90 GC patients who underwent surgery were collected before and one week after the surgery. Thirty GC and matched normal tissues were sampled from patients who had undergone surgical resection. The plasma level of UCA1 was quantified using RT-qPCR. In situ hybridization was carried out on formaldehyde-fixed tissue sections from GC patients to detect UCA1. Cell migration assay, cell proliferation assay, and flow cytometry analysis were carried out to study the effect of UCA1 on GC development in vitro. RT-PCR results showed that the expression levels of UCA1 in GC tissues were significantly higher compared to those in adjacent normal specimens. Down-regulation of UCA1 inhibited the proliferation, migration, and apoptosis of GC cells. In GC patients, plasma expression of UCA1 was significantly up-regulated compared to that in healthy controls (1.417 ± 0.106 vs. 0.223 ± 0.030, p < 0.0001). Plasma UCA1 was significantly correlated with tumor differentiation (p < 0.05), T stage (p < 0.001) and lymph node metastasis (p < 0.001). Plasma UCA1 expression (AUC = 0.883) in post-surgery samples was significantly decreased compared to the expression level of pre-surgery patients (1.403 ± 1.329 versus 0.712 ± 0.944, p < 0.01). UCA1 promoted proliferation, migration and apoptosis of GC cells and was significantly up-regulated in GC plasma, indicating poor tumor prognosis.

Overexpression of LncRNA-UCA1 Correlates with Lung Adenocarcinoma Progression and Poor Prognosis.

Long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been predicted to play a critical role in various biological processes including tumorigenesis. However, the clinical significance of UCA1 in lung adenocarcinoma (LUAD) is still not understood in detail. The aim of this study was to assess the clinical significance of the UCA1 expression levels in LUAD based on publicly available data and to evaluate its potential signaling pathways. The RNA-sequencing (RNA-seq) dataset and clinical information of all LUAD patients were downloaded from The Cancer Genome Atlas (TCGA). Kaplan-Meier plot and log-rank test were performed for survival analysis; Cox proportional hazards regression model were used to assess the relative factors. Furthermore, Starbase, Cbioportal, and Multi Experiment Matrix starbases were used to identify UCA1-related genes in LUAD. Finally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of UCA1-related genes were performed using DAVID. The expression level of UCA1 in LUAD tissues (n = 468) was significantly increased compared with the adjacent non-tumor lung tissues (n = 52) (p < 0.0001). In addition, UCA1 level was significantly correlated with TNM stage and lymph node metastasis. Survival analysis showed that UCA1 over-expression was significantly associated with poor overall survival (OS) (p = 0.0098) and poor recurrence-free survival (RFS) (p = 0.0298) in LUAD patients. Multivariate analysis confirmed that high expression of lncRNA-UCA1 was an independent prognostic factor of poor OS (HR = 1.353, 95% CI: 1.005 - 1.822, p = 0.046). Finally, KEGG analysis for UCA1-related genes indicated that UCA1 might be enriched with the microRNAs in cancer, pathways in cancer, endocytosis, focal adhesion, and proteoglycans in cancer. This study showed that UCA1 may be involved in lung carcinogenesis, which could act as a biomarker of prognosis and therapeutic target in LUAD patients.

Knockdown of long noncoding RNA urothelial carcinoma-associated 1 inhibits cell viability, migration, and invasion by regulating microRNA-182 in gastric carcinoma.

Long noncoding RNA urothelial carcinoma-associated 1 (UCA1) has been reported to be a vital mediator in various cancers. But, in terms of gastric cancer (GC), the effects of UCA1 on GC cell proliferation, migration, invasion, and apoptosis remain unclear. This study aimed to uncover the potential regulatory mechanism of UCA1 in GC cells. The expression level of UCA1 was first examined in the five different cell lines of HEK293, CCL-153, HUVEC, SUN-216, and SGC-7901 using a reverse-transcriptase quantitative polymerase chain reaction. Then, the vectors of short hairpin UCA1, the microRNA-182 (miR-182) mimic/inhibitor, and the pEX-tissue inhibitor of metalloproteinases 2 (TIMP2)/small interfering TIMP2 were transfected into SUN-216 and SGC-7901 cells to alter UCA1, miR-182, and TIMP2 expression. To investigate the biological functions, cell viability, migration, invasion, and apoptosis were examined by Cell Counting Kit-8, Transwell, and flow cytometry. The key factors of apoptosis and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase 3β (GSK3β) and nuclear factor κB (NF-κB) signal pathways were determined by Western blot analysis. UCA1 was upregulated in SUN-216 and SGC-7901 cells than in the other three cell lines of HEK293, CCL-153, and HUVEC. Knockdown of UCA1 significantly suppressed cell viability, migration, and invasion, and promoted apoptosis by regulating B-cell lymphoma 2, Bax, and cleaved-caspase-3/9 expressions. However, miR-182 overexpression markedly reversed the regulatory effect of UCA1 knockdown on SUN-216 and SGC-7901 cells. TIMP2 was a direct target gene of miR-182, and TIMP2 overexpression exhibited the same effect of UCA1 knockdown on cell viability, migration, invasion, and apoptosis. Besides, miR-182 activated PI3K/AKT/GSK3β and NF-κB signal pathways by regulation of TIMP2. Knockdown of UCA1 exerts an anticancer effect on GC cells by regulating miR-182.

Long noncoding RNA UCA1 promotes anaplastic thyroid cancer cell proliferation via miR‑135a‑mediated c‑myc activation.

The long non‑coding RNA (lncRNA), urothelial carcinoma‑associated 1 (UCA1), has been demonstrated to be dysregulated and serves a role in the progression of several cancer types. However, the exact effects and underlying molecular mechanisms of UCA1 in anaplastic thyroid cancer (ATC) remain unknown. The aim of the present study was to investigate the detailed function and the mechanism of UCA1 in the regulation of ATC cell progression. The present study identified that the expression levels of UCA1, in ATC cell lines and tissues, were significantly upregulated compared with normal human thyroid cell line and adjacent non‑cancerous tissues, respectively. UCA1 knockdown significantly inhibited ATC cell viability, proliferation, migration and invasion and the expression level of c‑myc proto‑oncogene (c‑myc) invitro, and suppressed ATC tumor growth invivo. In addition, using luciferase assays, it was confirmed that miR‑135a directly bound to UCA1 and the 3' untranslated region of c‑myc, and UCA1 competed with c‑myc for miR‑135a binding. miR‑135a inhibition may upregulate c‑myc expression, however, the upregulation of c‑myc may be partially reduced by short hairpin UCA1. The present results illustrated that UCA1 promoted ATC cell proliferation through acting as a competing endogenous RNA by binding miR‑135a. In conclusion, in the present study, UCA1 served as an oncogenic long non‑coding RNA promoting ATC cell proliferation and may be a potential target for human ATC treatment.

Long non‑coding RNA UCA1 promotes papillary thyroid cancer cell proliferation via miR‑204‑mediated BRD4 activation.

Long non‑coding RNA (lncRNA) urothelial carcinoma‑associated 1 (UCA1) has been used in tumor development and progression in many types of cancer. However, the function and mechanism underlying the action of UCA1 in papillary thyroid cancer (PTC) remains unclear. Therefore, these topics were investigated in the present study by invitro and invivo experiments. It was demonstrated that the expression level of UCA1 was more significantly upregulated in PTC cell lines and tissues when compared with the immortal human thyroid follicular cell line and adjacent normal tissues, respectively. UCA1 knockdown significantly inhibited PTC cell viability, colony formation and the bromodomain containing 4 (BRD4) expression level invitro, and retarded PTC tumor growth invivo. In the previous study, microRNA (miR)‑204 inhibited thyroid cancer progression and was regulated by UCA1 in other types of cancer. In addition, by conducting dual luciferase reporter assays, it was confirmed that miR‑204 directly binds to UCA1 and the 3'‑untranslated region of BRD4. Furthermore, UCA1 competed with BRD4 for miR‑204 binding. miR‑204 knockdown enhanced BRD4 expression, which can be partially restored by short hairpin‑UCA1. The results of the present study illustrated that UCA1 promotes PTC progression by acting as a competing endogenous RNA by sponging miR‑204. In conclusion, UCA1 may be regarded as an oncogenic lncRNA, promoting PTC cell proliferation, and be a potential target for human PTC treatment.

Expression of long non-coding RNA UCA1 and miR-34b in bladder cancer and analysis of clinic-pathologic correlation

Objective To study the expression of long non-coding RNA (lncRNA)- urothelial carcinoma associated 1(UCA1) and miR-34b in bladder cancer and its correlation to the clinicopathologic features of bladder cancer. Methods Between January 2011 and October 2012 , the expression of UCA1 and miR-34b in 5 bladder cancer cell lines (T24, BIU-87, EJ, T24-MMC, T24-ADM)and 1 normal bladder cell lines (SV-HUC-1) were measured by real-time reverse transcription-polymerase chain reaction (RT-PCR). Meanwhile, the 56 bladder cancer specimens and paraneoplastic normal bladder tissues, which diagnosed by pathology were collected from bladder cancer patients undergoing radical resection of bladder. Among them, 41 cases were male and 15 cases were female. The mean age was (68.4±7.5)years old, range 52 to 78 years.43 cases were older than 65 years old, and 13 cases were less than 65 years old. The pathological classification included non muscle-invasive bladder cancer (NMIBC) 18 cases, muscle-invasive bladder cancer 38 cases; low grade papillary urothelial carcinoma 22 cases, high grade papillary urothelial carcinoma 34 cases; 12 cases were primary lesion, the other 44 cases were diagnosed as tumor recurrence. Real-time RT-PCR was performed to analyze the expression of UCA1 and miR-34b. Results The relative expression levels of UCA1 in the normal bladder cell lines (SV-HUC-1) and 5 bladder cancer cell lines (T24, BIU-87, EJ, T24-MMC and T24-ADM)were (0.0675±0.0133), (0.2934±0.0531), (0.4246±0.0650), (0.4206±0.0826), (0.6472±0.0875) and (0.7165±0.1032), respectively (P<0.05). Moreover, the expression levels of UCA1 were up-regulated in 2 drug resistant bladder cancer cells lines T24-MMC(0.6472±0.0875)and T24-ADM(0.7165±0.1032), as compared with the T24 bladder cancer lines (0.2934±0.0531) , respectively (P<0.05). However, the expression levels of miR-34b in 5 bladder cancer cell lines [T24(0.1600±0.0455), BIU-87(0.1720±0.0658), EJ(0.1150±0.0352), T24-MMC(0.0576±0.0087), T24-ADM(0.0510±0.0125)]were decreased(P<0.05), as compared with normal bladder cell lines SV-HUC-1(0.6384±0.1083). Moreover, the expression levels of miR-34b were down-regulated in 2 drug resistant bladder cancer cells lines T24-MMC(0.0576±0.0087)and T24-ADM(0.0510±0.0125), as compared with the T24 bladder cancer lines T24(0.1600±0.0455), respectively (P<0.05). The relative expression levels of UCA1 and miR-34b in bladder cancer tissues and paraneoplastic normal bladder tissues were (0.4225±0.0714)vs.(0.0532±0.0192)and(0.0340±0.0134)vs.(0.5643±0.0616), respectively (P<0.05). Statistical correlation analysis showed that UCA1 to be significantly negative correlated with miR-34b in bladder cancer specimens(r=-0.54, P<0.05). The high level of UCA1 and low level of miR-34b were significantly correlated with tumor malignant grade, invasiveness and recurrence. The 3-year overall survival rate (OS) in UCA1(+ )/miR-34b(-) group (27.6%) were significantly worse compared with non UCA1(+ )/miR-34b(-) group(73.7%). Conclusion High expression of UCA1 and low expression of miR-34b were associated with the occurrence and development of bladder cancer. Key words: Urinary bladder neoplasms; Long non-coding RNA; Urothelial carcinoma associated 1; MicoRNAs

Identification of long-non coding RNA UCA1 as an oncogene in renal cell carcinoma

Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults, which is associated with poor prognosis and high recurrence. Long non‑coding RNAs (lncRNAs) have been reported to be dysregulated in cancer and to be important in the regulation of carcinogenesis, thus suggesting that this class of molecules may be used as biomarkers in cancer. The lncRNA urothelial carcinoma associated 1 (UCA1) has been observed to be upregulated and to function as an oncogene in certain types of cancer; however, the role of UCA1 in RCC remains to be elucidated. The present study aimed to determine the expression and function of UCA1 in RCC. Quantitative polymerase chain reaction (qPCR) was used to determine the expression levels of UCA1 in 46 paired RCC and adjacent normal tissue samples. Furthermore, qPCR was used to determine the expression levels of UCA1 in four RCC cell lines compared with the human embryonic kidney 293T cell line. The impact of UCA1 on cell migration, proliferation and apoptosis was investigated by wound scratch assay, MTT and flow cytometry, respectively. The results of the present study demonstrated that UCA1 expression levels were significantly increased in RCC tissues and cells, as compared with the controls. Ectopic expression and gene silencing of UCA1 in RCC cell lines exerted opposite effects on cellular proliferation, migration and apoptosis, and the results suggested that UCA1 may function as an oncogene in RCC. These results indicated that UCA1 may be considered as a promising biomarker for diagnosis, and a therapeutic target in RCC. Further research is required to elucidate the role and target genes of UCA1 in RCC.

UCA1 overexpression predicts clinical outcome of patients with ovarian cancer receiving adjuvant chemotherapy.

Urothelial carcinoma associated 1 (UCA1) functions as an oncogene, which promotes cancer cell proliferation, invasion, and metastasis, and is responsible for drug resistance. This study aimed to determine the expression level of UCA1 in ovarian cancer and to further investigate its clinical significance. The expression levels of UCA1 in ovarian cancer and normal ovaries were determined by quantitative real-time PCR. The relationship between UCA1 expression and clinical features and the prognostic value of UCA1 for overall survival were examined. UCA1 expression in ovarian cancer tissues was significantly upregulated compared with normal ovarian tissues. High UCA1 expression was related to lymph node metastasis, FIGO stage, and response to chemotherapy. Kaplan-Meier analysis demonstrated that high UCA1 expression was associated with poorer overall survival in patients with ovarian cancer. Cox proportional hazards analysis showed that high UCA1 expression was an independent prognostic marker of poor outcome. This effect remained significant in the further stratification analysis. Our findings provided the first evidence that UCA1 may serve as an indicator of response to chemotherapy and prognosis of ovarian cancer. UCA1 may play an important role in the progression of ovarian cancer.

UCA1, a long noncoding RNA, promotes the proliferation of CRC cells via p53/p21 signaling

AbstractObjectiveRecently, the role of long noncoding RNAs (lncRNAs) in human colorectal cancer (CRC) has been a subject of intense focus. We set out to determine the function of one lncRNA, termed urothelial carcinoma-associated 1 (UCA1) in CRC cell proliferation and its underlying mechanisms.MethodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expression level of UCA1 in 50 pairs of CRC samples compared with non-tumor colon tissues. Cell growth was determined using the Cell Counting Kit-8 (CCK-8). Western blotting was carried out to analyze the related protein expression. Flow cytometry was done to evaluate cell apoptosis by UCA1 inhibition.ResultsWe found an increased expression of UCA1 in CRC samples. Knockdown of UCA1 in HCT116 cells induced a decrease in cell proliferation rate compared to control samples. This oncogenic activity may be enhanced through p53/ p21 signaling.ConclusionOur results supported the hypothesis that upregulation of UCA1 contributes to the unlimited proliferation rate of CRC cells, at least partially through the negative regulation of p53/p21 signaling pathway. Finally, we found that UCA1 merely influenced CRC cell apoptosis.