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Background UCA1 is a long non-coding RNA which was found overexpressed in various human cancers including gastric cancer (GC). It is identified that UCA1 promotes GC cells proliferation, migration and invasion, however, the role of UCA1 during the processes of immune escape is still not unclear. Methods We collected 40 paired GC and non-tumor tissue samples. The level of UCA1 in GC and control tissue samples were determined by in situ hybridization and qRT-PCR. Cell viability was determined by MTT assay. GC cells’ migration capacities were examined by transwell assay. To understand the roles of UCA1 during immune escape, wildtype or UCA1 KO GC cells co-cultured with peripheral blood mononuclear cells or cytokine-induced killer cells in vitro. Mouse model was used to examine the function of UCA1 in vivo. Results UCA1 promoted GC cells proliferation and migration, and inhibit apoptosis. UCA1 repressed miR-26a/b, miR-193a and miR-214 expression through direct interaction and then up-regulated the expression of PDL1. UCA1-KO GC cells could induce a higher IFNγ expression when co-cultured with peripheral blood mononuclear cells (PBMCs), and have a lower survival rate when co-cultured with cytokine-induced killer (CIK) cells in vitro. UCA1-KO GC cells formed smaller tumors, had higher miR-26a, −26b, −193a and − 214 level, reduced cell proliferation and increased apoptosis in xenograft mouse model. Conclusions UCA1 overexpression protected PDL1 expression from the repression of miRNAs and contributed to the GC cells immune escape. UCA1 could serve as a potential novel therapeutic target for GC treatment.

Long noncoding RNAs (lncRNAs), longer than 200 nucleotides in length, play important roles in the development and progression of various cancers. An increasing number of studies have revealed that lncRNAs function as potential oncogenes or tumor suppressors to influence biological processes, such as cell growth, invasion, migration and apoptosis. Urothelial carcinoma associated 1 (UCA1), an oncogenic lncRNA, was first found in bladder cancer and highly expressed in multiple cancers, including gastric cancer, colorectal cancer, lung cancer and breast cancer. UCA1 promotes tumorigenesis mainly via binding to tumor-suppressive microRNAs (miRNAs), activating several pivotal signaling pathways and alteration of epigenetic and transcriptional regulation. In addition, high expression of UCA1 is related to poor clinicopathological features especially for shorter overall survival, suggesting that UCA1 might be regarded as a prognosis biomarker in human cancers. In the present review, we summarized current studies on UCA1 to explore its prognostic value and underlying regulation mechanisms in the development of multiple cancers in order to provide a glimmer of hope for the prevention and treatment of malignant tumors.Long noncoding RNAs (lncRNAs), longer than 200 nucleotides in length, play important roles in the development and progression of various cancers. An increasing number of studies have revealed that lncRNAs function as potential oncogenes or tumor suppressors to influence biological processes, such as cell growth, invasion, migration and apoptosis. Urothelial carcinoma associated 1 (UCA1), an oncogenic lncRNA, was first found in bladder cancer and highly expressed in multiple cancers, including gastric cancer, colorectal cancer, lung cancer and breast cancer. UCA1 promotes tumorigenesis mainly via binding to tumor-suppressive microRNAs (miRNAs), activating several pivotal signaling pathways and alteration of epigenetic and transcriptional regulation. In addition, high expression of UCA1 is related to poor clinicopathological features especially for shorter overall survival, suggesting that UCA1 might be regarded as a prognosis biomarker in human cancers. In the present review, we summarized current studies on UCA1 to explore its prognostic value and underlying regulation mechanisms in the development of multiple cancers in order to provide a glimmer of hope for the prevention and treatment of malignant tumors.

Background To overcome the hostile hypoxic microenvironment of solid tumors, tumor cells secrete a large number of non-coding RNA-containing exosomes that facilitate tumor development and metastasis. However, the precise mechanisms of tumor cell-derived exosomes during hypoxia are unknown. Here, we aim to clarify whether hypoxia affects tumor growth and progression by transferring long non-coding RNA-urothelial cancer-associated 1 (lncRNA-UCA1) enriched exosomes secreted from bladder cancer cells. Methods We used bladder cancer 5637 cells with high expression of lncRNA-UCA1 as exosome-generating cells and bladder cancer UMUC2 cells with low expression of lncRNA-UCA1 as recipient cells. Exosomes derived from 5637 cells cultured under normoxic or hypoxic conditions were isolated and identified by transmission electron microscopy, nanoparticle tracking analysis and western blotting analysis. These exosomes were co-cultured with UMUC2 cells to evaluate cell proliferation, migration and invasion. We further investigated the roles of exosomal lncRNA-UCA1 derived from hypoxic 5637 cells by xenograft models. The availability of lncRNA-UCA1 in serum-derived exosomes as a biomarker for bladder cancer was also assessed. Results We found that hypoxic exosomes derived from 5637 cells promoted cell proliferation, migration and invasion, and hypoxic exosomal RNAs could be internalized by three bladder cancer cell lines. Importantly, lncRNA-UCA1 was secreted in hypoxic 5637 cell-derived exosomes. Compared with normoxic exosomes, hypoxic exosomes derived from 5637 cells showed the higher expression levels of lncRNA-UCA1. Moreover, Hypoxic exosomal lncRNA-UCA1 could promote tumor growth and progression though epithelial-mesenchymal transition, in vitro and in vivo. In addition, the expression levels of lncRNA-UCA1 in the human serum-derived exosomes of bladder cancer patients were higher than that in the healthy controls. Conclusion Together, our results demonstrate that hypoxic bladder cancer cells remodel tumor microenvironment to facilitate tumor growth and development though secreting the oncogenic lncRNA-UCA1-enriched exosomes and exosomal lncRNA-UCA1 in human serum has the possibility as a diagnostic biomarker for bladder cancer.

The aim of this study was to explore the roles of the long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) on cisplatin resistance in ovarian cancer and the underlying mechanisms. We investigated the expression of lncRNAs in 3 paired cisplatin-sensitive and cisplatin-resistant tissues of ovarian cancer by microarray analysis. The qRT-PCR analysis was to investigate the expression pattern of UCA1 in cisplatin-resistant ovarian cancer patient tissues and cell lines. Then we examined the effects of UCA1 on cisplatin resistance in vitro and in vivo. In this study, UCA1 was observed to be upregulated in cisplatin-resistant patient tissues and cell lines. Knockdown of UCA1 inhibited cell proliferation and promoted the cisplatin-induced cell apoptosis in ovarian cancer cells. Then we demonstrated that repressed UCA1 promoted the miR-143 expression and miR-143 could bind to the predicted binding site of UCA1. Furthermore, we found that miR-143 displayed its role via modulating the FOSL2 expression. Importantly, we demonstrated that UCA1 was upregulated in serum exosomes from cisplatin-resistant patients. In summary, our study demonstrated that UCA1 modulates cisplatin resistance through the miR-143/FOSL2 pathway in ovarian cancer.

Within the non-coding genome landscape, long non-coding RNAs (lncRNAs) and their secretion within exosomes are a window that could further explain the regulation, the sustaining, and the spread of lung diseases. We present here a compilation of the current knowledge on lncRNAs commonly found in Chronic Obstructive Pulmonary Disease (COPD), asthma, Idiopathic Pulmonary Fibrosis (IPF), or lung cancers. We built interaction networks describing the mechanisms of action for COPD, asthma, and IPF, as well as private networks for H19, MALAT1, MEG3, FENDRR, CDKN2B-AS1, TUG1, HOTAIR, and GAS5 lncRNAs in lung cancers. We identified five signaling pathways targeted by these eight lncRNAs over the lung diseases mentioned above. These lncRNAs were involved in ten treatment resistances in lung cancers, with HOTAIR being itself described in seven resistances. Besides, five of them were previously described as promising biomarkers for the diagnosis and prognosis of asthma, COPD, and lung cancers. Additionally, we describe the exosomal-based studies on H19, MALAT1, HOTAIR, GAS5, UCA1, lnc-MMP2-2, GAPLINC, TBILA, AGAP2-AS1, and SOX2-OT. This review concludes on the need for additional studies describing the lncRNA mechanisms of action and confirming their potential as biomarkers, as well as their involvement in resistance to treatment, especially in non-cancerous lung diseases.

Cancer cells preferentially metabolize glucose through aerobic glycolysis, a phenomenon known as the Warburg effect. Emerging evidence has shown that long non‐coding RNAs (lncRNAs) act as key regulators of multiple cancers. However, it remains largely unexplored whether and how lncRNA regulates glucose metabolism in cancer cells. In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1‐induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. Taken together, these findings provide the first evidence that UCA1 plays a positive role in cancer cell glucose metabolism through the cascade of mTOR–STAT3/microRNA143–HK2, and reveal a novel link between lncRNA and the altered glucose metabolism in cancer cells. UCA1 plays a positive role in cancer cell glucose metabolism. UCA1 exerts its role in glycolysis through the cascade of mTOR‐STAT3/miR143‐HK2.

: Drug resistance of cancer cells is one of the major causes of chemotherapy failure. Recently research demonstrated that long non-coding RNA Urothelial cancer associated 1 (UCA1) could promote tumor cisplatin resistance. In this study, we aim to investigate the role of UCA1 in the cisplatin treatment of gastric cancer and its underlying mechanism. : Cell counting kit-8 (CCK-8) assay and apoptosis assay were used to detect the effects of different doses of cisplatin on the proliferation and apoptosis of gastric cancer. We examined the expression relationship between the Enhancer of Zeste Homologue 2 (EZH2) and UCA1 by quantitative Real-time polymerase chain reaction (qRT-PCR) and western blot analysis. Western blot analysis was also performed to detect the expression levels of apoptosis-related proteins, EZH2 and key genes in PI3K/AKT signaling pathway, RIP and RNA pull down assays were performed to explore the interaction between UCA1 and EZH2. : We demonstrated that higher the UCA1 expression levels in GC tissues correlated with the poorer the prognosis of patients according to the TCGA database, the GEO database. Moreover, overexpression of UCA1 promotes GC cell proliferation and inhibits cisplatin-induced apoptosis. Knockdown of UCA1 showed the opposite results. Besides, UCA1 exerted its function through interacting with EZH2 and regulates EZH2 expression, knockdown of EZH2 decreased cisplatin resistance of GC cells. Hence, UCA1 promotes cisplatin resistance of GC via recruiting EZH2 and activating PI3K/AKT pathway. : Our research revealed the lncRNA UCA1 promoted the cisplatin resistance of GC by recruiting EZH2 and activating PI3K/AKT pathway to modulate cell apoptosis, indicating treatments targeting UCA1 or EZH2 might provide meaningful therapeutic strategies for cisplatin-resistance GC patients.

Background Accumulating literatures have indicated that long non-coding RNAs (lncRNAs) are potential biomarkers that play key roles in tumor development and progression. Urothelial cancer associated 1 (UCA1) is a novel lncRNA that acts as a potential biomarker and is involved in the development of cancers. However, the molecular mechanism of UCA1 in renal cancer is still needed to further explore. Methods The relative expression level of UCA1 was determined by Real-Time qPCR in a total of 88 patients with urothelial renal cancer and in different renal cancer cell lines. Loss-of-function experiments were performed to investigate the biological roles of UCA1 and miR-182-5p on renal cancer cell proliferation, migration, apoptosis and tumorigenicity. Comprehensive transcriptional analysis, dual-luciferase reporter assay and western blot etc. were performed to explore the molecular mechanisms underlying the functions of UCA1. Results In this study, we found that UCA1 was significantly up-regulated in renal cancer. Moreover, increased UCA1 expression was positively correlated with differentiation and advanced TNM stage. Further experiments demonstrated that knockdown of UCA1 inhibited malignant phenotypes and Notch signal path of renal cancer cells, and miR-182-5p was reverse function as UCA1. UCA1 functioned as a miRNA sponge to positively regulate the expression of Delta-like ligand 4(DLL4) through sponging miR-182-5p and subsequently promoted malignant phenotypes of renal cancer cells, thus UCA1 playing an oncogenic role and miR-182-5p as an antioncogenic one in renal cancer pathogenesis. Conclusion UCA1-miR-182-5p-DLL4 axis is involved in proliferation and progression of renal cancer. Thus, this study demonstrated that UCA1 plays a critical regulatory role in renal cancer cell and UCA1 may serve as a potential diagnostic biomarker and therapeutic target of renal cancer.

With the development of functional genomics studies, a mass of long non‐coding RNAs (LncRNA) were discovered from the human genome. Long non‐coding RNAs serve as pivotal regulators of genes that are able to generate LncRNA–binding protein complexes to modulate a great number of genes. Recently, the LncRNA urothelial carcinoma‐associated 1 (UCA1) has been revealed to be dysregulated, which plays a critical role in the development of a few cancers. However, the role of the biology and clinical significance of UCA1 in the tumorigenesis of oral squamous cell carcinoma (OSCC) remain unknown. We found that UCA1 expression levels were upregulated aberrantly in tongue squamous cell carcinoma tissues and associated with lymph node metastasis and TNM stage. We explored the expression, function, and molecular mechanism of LncRNA UCA1 in OSCC. In the present work, we revealed that UCA1 silencing suppressed proliferation and metastasis and induced apoptosis of OSCC cell lines in vitro and in vivo, which might be related to the activation level of the WNT/β‐catenin signaling pathway. Our research results emphasize the pivotal role of UCA1 in the oncogenesis of OSCC and reveal a novel LncRNA UCA1–β‐catenin–WNT signaling pathway regulatory network that could contribute to our understanding in the pathogenesis of OSCC and assist in the discovery of a viable LncRNA‐directed diagnostic and therapeutic strategy for this fatal disease. Our data highlighted the pivotal role of UCA1 in the tumorigenesis of oral squamous cell carcinoma, and revealed a novel LncRNA UCA1‐β‐catenin‐Wnt signaling pathway regulatory network, which may contribute to understand the pathogenesis of oral squamous cell carcinoma.

Background Urothelial cancer associated 1 (UCA1) is a long noncoding RNA (lncRNA) which has gained more attention in recent years due to its aberrant expression in embryogenesis and a broad range of cancer tissues and cells. Importantly, multiple studies have shown that UCA1 plays oncogenic roles in tumor growth and metastasis, and it may act as a potential biomarker and therapeutic target for human cancers. However, the molecular mechanism of UCA1 in cancer initiation, progression and metastasis remains incompletely understood. Thus, gaining a better understanding of the functional mechanism of UCA1 in cancer onset and progression is of the utmost significance for evaluating the potential application of UCA1. Results and discussion In this review, we discuss UCA1 expression profiling, isoform, expression regulation, biological role and mechanism for UCA1 tumor-promoting effect. We further discuss the potential clinical application of UCA1 as a promising diagnostic biomarker or therapeutic target for human cancers. Conclusion UCA1 functions as an oncogenic lncRNA in several malignancies, and it might become a potential biomarker or therapeutic target for human cancers.