lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer

Jiao, Changjie; Song, Zhiming; Chen, Jianming; Zhong, Jue; Cai, Weibin; Tian, Suke; Chen, Songlin; Yi, Yongxiang; Xiao, Yun

doi:10.3892/or.2016.5121

Cited by 91 publications

(82 citation statements)

References 37 publications

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“…Moreover, miR-195 directly suppressed ARL2 mRNA and protein levels in bladder tumor cells, indicating that miR-195 may be a tumor suppressor gene that decreases ARL2 expression in BC. Additionally, it has been reported that ARL2 expression was directly regulated by miR-195 in human neural progenitor cells [20]. These findings suggest that ARL2 is in turn negatively regulated by miR-195.…”

Section: Discussionsupporting

confidence: 55%

“…Moreover, UCA1 functions as a ceRNA of miR-16 to contribute to imatinib resistance in chronic myeloid leukemia cells [19]. In addition, UCA1 promotes cellular proliferation by acting as a ceRNA against Sox4 in esophageal cancer [20]. Therefore, we hypothesized that UCA1 can also acts as a decoy miRNA in regulation of mitochondrial function in BC.…”

Section: Discussionmentioning

confidence: 99%

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LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway

Sun

et al. 2017

Cell Physiol Biochem

102

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Background/Aims: This study aims to identify whether Urothelial Cancer Associated 1 (UCA1) regulates mitochondrial metabolic reprogramming in bladder cancer, and to explore how UCA1 participates in mitochondrial metabolism by the UCA1/miR-195/ARL2 signaling pathway; these findings may be aid in the development of tumor diagnostic and therapeutic strategies. Methods: Bladder tissues were obtained from patients. Stable cell lines were constructed, with ectopic expression of UCA1 in UMUC2 cells and knockdown of UCA1 in 5637 cells. The expression levels of UCA1, miR-195, and ARL2 were detected by real-time PCR, western blotting, and immunohistochemistry Cell viability was detected by Cell Counting Kit-8 (CCK8) assay; mitochondrial DNA copy numbers were tested by realtime PCR; ATP level was evaluated by ATP assay kit; mitochondrial membrane potential was analyzed by 5,5’,6,6’-tetrachloro-1,1’,3,3’- tetraethylbenzimidazolylcarbocyanine iodide (JC-1) fluorescent probe. miRNAs between UCA1 and ARL2 were predicted by TargetScan and RNAHybrid, and then determined by real-time PCR. Dual-luciferase activity assay and RNA immunoprecipitation (RIP) assay were used to verify the relationship between UCA1 and miR-195. The expression level of ARL2 was silenced by small interfering RNA(siRNA). For in vivo experiments, UCA1-silencing 5637 cells were subcutaneously injected into BALB/C nude mice to evaluate the effects of UCA1 on tumor progression by the regulation of miR-195 and ARL2. Results: We demonstrate here that UCA1 enhances mitochondrial function in bladder cancer cells. UCA1 contributes to ARL2-induced mitochondrial activity, which plays an important role in mitochondrial function. UCA1, as a competing endogenous RNA (ceRNA), regulates mitochondrial function through upregulating ARL2. In this way, it inhibited the miR-195 signaling pathway to enhance mitochondrial function in bladder cancer. Additionally, ARL2 is a direct target of miR-195 and can be repressed by either miR-195 overexpression or UCA1 inhibition. Knockdown of ARL2 was analogous to the inhibition of UCA1 and the upregulation of miR-195. Animal experiments further indicated that UCA1 promoted bladder tumor growth by regulating miR-195 /ARL2. Conclusion: These data suggest that UCA1 enhanced mitochondrial function and cell viability through the UCA1/miR-195/ARL2 axis in vitro and in vivo. The elucidation of this signaling network provides a more adequate theoretical basis for understanding the molecular pathology of bladder cancer, and also UCA1 as a potential diagnosis and treatment target for bladder cancer.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway

Sun

et al. 2017

Cell Physiol Biochem

102

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“…For example, Jiao et al showed that lncRNA UCA1 enhanced cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer [12]. Lv et al showed that lncRNA Unigene56159 promoted epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells [13].…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: LncRNA NEAT1 regulates epithelial-mesenchymal transition of osteosarcoma by miR-186-5p as competing endogenous RNA

H¹,

Zhao²

2017

Oncotarget

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Increasing evidence showed that lncRNA NEAT1 play important roles in regulating tumor carcinogenesis and progression. However, the function and underlying mechanism of NEAT1 in osteosarcoma (OS) remain unclear. In the present study, we found that NEAT1 expression was significantly upregulated in OS tissues and cell lines. High NEAT1 expression was closely associated with advanced clinicopathologic features and poor overall survival of OS patients. In vitro function assay, we found that NEAT1 could promote OS cells proliferation, invasion, and epithelial-mesenchymal transition (EMT) process. NEAT1 could also promote OS cells growth in vivo. In addition, our studies showed that miR-186-5p was a downstream target of NEAT1 in OS. Functionally, miR-186-5p suppressed OS cells proliferation, invasion, and EMT process. Furthermore, our data revealed that HIF-1α was a downstream target of miR-186-5p and NEAT1 could exert its tumor oncogenic roles on OS cells via miR-186-5p/ HIF-1α axis. Taken together, we elucidated that the NEAT1/miR-186-5p/HIF-1α axis might be a therapeutic approach for the treatment of OS.

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“…According to the criteria for selection mentioned above, after carefully screening the abstract and full-text of these references, finally, 14 publications (including 15 studies) [16–29] were identified as eligible for the present quantitative analysis of the prognostic value of UCA1 in digestive system cancers. All included publications were written in English.…”

Section: Resultsmentioning

confidence: 99%

The prognostic significance of UCA1 for predicting clinical outcome in patients with digestive system malignancies

et al. 2017

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BackgroundUrothelial Carcinoma Associated 1 (UCA1) was an originally identified lncRNA in bladder cancer. Previous studies have reported that UCA1 played a significant role in various types of cancer. This study aimed to clarify the prognostic value of UCA1 in digestive system cancers.ResultsThe meta-analysis of 15 studies were included, comprising 1441 patients with digestive system cancers. The pooled results of 14 studies indicated that high expression of UCA1 was significantly associated with poorer OS in patients with digestive system cancers (HR: 1.89, 95 % CI: 1.52–2.26). In addition, UCA1 could be as an independent prognostic factor for predicting OS of patients (HR: 1.85, 95 % CI: 1.45–2.25). The pooled results of 3 studies indicated a significant association between UCA1 and DFS in patients with digestive system cancers (HR = 2.50; 95 % CI = 1.30–3.69). Statistical significance was also observed in subgroup meta-analysis. Furthermore, the clinicopathological values of UCA1 were discussed in esophageal cancer, colorectal cancer and pancreatic cancer.Materials and methodsA comprehensive retrieval was performed to search studies evaluating the prognostic value of UCA1 in digestive system cancers. Many databases were involved, including PubMed, Web of Science, Embase and Chinese National Knowledge Infrastructure and Wanfang database. Quantitative meta-analysis was performed with standard statistical methods and the prognostic significance of UCA1 in digestive system cancers was qualified.ConclusionsElevated level of UCA1 indicated the poor clinical outcome for patients with digestive system cancers. It may serve as a new biomarker related to prognosis in digestive system cancers.

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lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer

Cited by 91 publications

References 37 publications

LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway

LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway

WITHDRAWN: LncRNA NEAT1 regulates epithelial-mesenchymal transition of osteosarcoma by miR-186-5p as competing endogenous RNA

The prognostic significance of UCA1 for predicting clinical outcome in patients with digestive system malignancies

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