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Knockdown of lncRNA TP73-AS1 inhibits gastric cancer cell proliferation and invasion via the WNT/?-catenin signaling pathway.

ABSTRACT: Long non-coding RNAs (lncRNAs) function as tumor suppressors or oncogenes in tumor development and progression. The purpose of the present study was to investigate the clinical significance and functional role of lncRNA TP73-AS1 in gastric cancer (GC). Reverse transcription-quantitative polymerase chain reaction analysis demonstrated that TP73-AS1 was significantly upregulated in GC tissues compared with adjacent normal tissues. The higher expression of TP73-AS1 was closely associated with lymph node metastasis and tumor-node-metastasis stage in patients with GC. Those patients with GC showing a higher expression of TP73-AS1 were predicted to have shorter disease-free survival and overall survival rates. The knockdown of TP73-AS1 was shown to markedly inhibit cell proliferation, cell colony formation and cell invasion. In addition, the downregulation of TP73-AS1 suppressed the expression of transcription factor 4 and ?-catenin, which suggested that a decrease in TP73-AS1 suppressed the WNT/?-catenin signaling pathway in GC. Therefore, these results indicated that TP73-AS1 may be a target for GC treatment.

SUBMITTER: Wang Y

PROVIDER: S-EPMC6096150 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature

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Knockdown of lncRNA TP73-AS1 inhibits gastric cancer cell proliferation and invasion via the WNT/β-catenin signaling pathway.

Wang Yufeng Y Xiao Shuai S Wang Bingyi B Li Yang Y Chen Quanning Q

Oncology letters 20180628 3

Long non-coding RNAs (lncRNAs) function as tumor suppressors or oncogenes in tumor development and progression. The purpose of the present study was to investigate the clinical significance and functional role of lncRNA TP73-AS1 in gastric cancer (GC). Reverse transcription-quantitative polymerase chain reaction analysis demonstrated that TP73-AS1 was significantly upregulated in GC tissues compared with adjacent normal tissues. The higher expression of TP73-AS1 was closely associated with lymph ...[more]

PMID: 30127921

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Project description:BackgroundLong non-coding RNAs (lncRNAs) are pervasively transcribed in genome and emerging as a new player in tumorigenesis due to their functions in transcriptional, posttranscriptional and epigenetic mechanisms of gene regulation. As the most frequent malignancy and the foremost source of cancer mortality, lung cancer is a heterogeneous disorder. The most common type of lung cancer is Non-small cell lung cancer (NSCLC), occupying 85% of the total cases, and the main subtypes of NSCLC include lung adenocarcinoma (LAD), large cell carcinoma (LCC), and lung squamous cell carcinoma (LSCC). Recently, numerous lncRNAs have been reported to be strongly linked to NSCLC. In the present study, we found that a new lncRNA CBR3-AS1 is highly expressed in lung cancer. In addition, we also examined the expression of lncRNA CBR3-AS1 in 60 of LADs, 40 of LCCs and 40 of LSCCs patient samples, finding that CBR3-AS1 was specificity highly expressed in LAD cancer tissues. Mechanically, we discovered that CBR3-AS1 could regulate the proliferation, migration and invasion of LAD cells through targeting Wnt/?-catenin signaling.MethodsReal-time PCR, RNA-pulldown, RIP, western blotting, lentivirus transfection, luciferase reporter assays, cell proliferation assays, colony formation assays, wound healing scratch assays and transwell assays were employed to examine the relationship between lncRNA CBR3-AS1 and its regulation of Wnt/?-catenin signaling in LAD cells.ResultsLncRNA CBR3-AS1 is highly-expressed in LAD and cell lines. LncRNA CBR3-AS1 shows physical association with ?-catenin. CBR3-AS1 could facilitate Wnt/?-catenin signaling activation thought promoting nuclear localization of ?-catenin. CBR3-AS1 promotes LAD cell proliferation, migration and invasion by targeting Wnt/?-catenin signaling.ConclusionIt can be found that a new functional lncRNA CBR3-AS1 could promote nuclear localization of ?-catenin so as to facilitate Wnt/?-catenin signaling activation and regulate the proliferation, migration and invasion of LAD cells.

Project description:BackgroundBladder cancer is the most common human urological malignancies with poor prognosis, and the pathophysiology of bladder cancer involves multi-linkages of regulatory networks in the bladder cancer cells. Recently, the long noncoding RNAs (lncRNAs) have been extensively studied for their role on bladder cancer progression. In this study, we evaluated the expression of DLX6 Antisense RNA 1 (DLX6-AS1) in the cancerous bladder tissues and studied the possible mechanisms of DLX6-AS1 in regulating bladder cancer progression.MethodsGene expression was determined by qRT-PCR; protein expression levels were evaluated by western blot assay; in vitro functional assays were used to determine cell proliferation, invasion and migration; nude mice were used to establish the tumor xenograft model.ResultsOur results showed the up-regulation of DLX6-AS1 in cancerous bladder cancer tissues and bladder cell lines, and high expression of DLX6-AS1 was correlated with advance TNM stage, lymphatic node metastasis and distant metastasis. The in vitro experimental data showed that DLX6-AS1 overexpression promoted bladder cancer cell growth, proliferation, invasion, migration and epithelial-to-mesenchymal transition (EMT); while DLX6-AS1 inhibition exerted tumor suppressive actions on bladder cancer cells. Further results showed that DLX6-AS1 overexpression increased the activity of Wnt/?-catenin signaling, and the oncogenic role of DLX6-AS1 in bladder cancer cells was abolished by the presence of XAV939. On the other hand, DLX6-AS1 knockdown suppressed the activity of Wnt/?-catenin signaling, and the tumor-suppressive effects of DLX6-AS1 knockdown partially attenuated by lithium chloride and SB-216763 pretreatment. The in vivo tumor growth study showed that DLX6-AS1 knockdown suppressed tumor growth of T24 cells and suppressed EMT and Wnt/?-catenin signaling in the tumor tissues.ConclusionCollectively, the present study for the first time identified the up-regulation of DLX6-AS1 in clinical bladder cancer tissues and in bladder cancer cell lines. The results from in vitro and in vivo assays implied that DLX6-AS1 exerted enhanced effects on bladder cancer cell proliferation, invasion and migration partly via modulating EMT and the activity of Wnt/?-catenin signaling pathway.

Dataset Information

Knockdown of lncRNA TP73-AS1 inhibits gastric cancer cell proliferation and invasion via the WNT/?-catenin signaling pathway.

Publications

Knockdown of lncRNA TP73-AS1 inhibits gastric cancer cell proliferation and invasion via the WNT/β-catenin signaling pathway.

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