Long Non-Coding RNA TUG1 as a Potential Novel Biomarker for Predicting the Clinical Outcome of Cancer Patients: a Meta-Analysis

Li, Boye; Shen, Sisi; Zhang, Wenmei; Qi, Tingjuan; Hu, Qin; Cheng, Yuan

doi:10.7754/clin.lab.2018.180520

Cited by 7 publications

(7 citation statements)

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“…As a new lncRNA that has just been discovered, TUG1 has been recognized as an oncogene in most cancers to involve in the regulation of cancer progression [26,27]. However, there are few studies on the molecular regulation mechanism of TUG1 on HCC.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

et al. 2020

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Background: Accumulating evidence indicates that the long noncoding RNA taurine upregulated gene 1(TUG1) plays a critical role in cancer progression and metastasis. However, the overall biological role and clinical significance of TUG1 in hepatocellular carcinoma (HCC) remain largely unknown. Methods:The expressions of TUG1, microRNA-216b-5p and distal-less homeobox 2 (DLX2) were detected by Quantitative real-time polymerase chain reaction (qRT-PCR). The target relationships were predicted by StarBase v.2.0 or TargetScan and confirmed by dual-luciferase reporter assay. The cell growth, apoptosis, migration and invasion were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Flow cytometry and Transwell assays, respectively. All protein expression levels were detected by western blot. Tumor xenografts were implemented to explore the role of TUG1 in vivo. Results:We found that there was a marked rise in TUG1 expression in HCC tissues and cells, and knockdown of TUG1 repressed the growth and metastasis and promoted apoptosis of HCC cells. In particular, TUG1 could act as a ceRNA, effectively becoming a sink for miR-216b-5p to fortify the expression of DLX2. Additionally, repression of TUG1 impared the progression of HCC cells by inhibiting DLX2 expression via sponging miR-216b-5p in vitro. More importantly, TUG1 knockdown inhibited HCC tumor growth in vivo through upregulating miR-216b-5p via inactivation of the DLX2.Conclusion: TUG1 interacting with miR-216b-5p contributed to proliferation, metastasis, tumorigenesis and retarded apoptosis by activation of DLX2 in HCC.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

et al. 2020

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“…Based on the clinical analysis, the association between TTN-AS1 expression and T Stage, lymphatic metastasis or TNM Stage was determined. Previous reports have focused on the prognostic value of lncRNAs in cancer patients [29,30]. It is unknown that whether TTN-AS1 can affect the prognosis of GC patients.…”

Section: Discussionmentioning

confidence: 99%

LncRNA TTN-AS1 contributes to gastric cancer progression by acting as a competing endogenous RNA of miR-376b-3p

Dong¹,

Peng²,

Yuan³

et al. 2019

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Long noncoding RNAs (lncRNAs) were reported to participate in the progression of gastric cancer (GC). However, little is known about the biological functions of TTN antisense RNA 1 (TTN-AS1) in GC. Using qRT-PCR examination, we found that TTN-AS1 was expressed at a higher level in GC tissues and cell lines compared to the normal controls. Kaplan-Meier analysis of GC patients revealed the negative correlation between TTN-AS1 expression and the overall survival. To detect the biological function of TTN-AS1 in GC, we silenced TTN-AS1 to perform loss-of-function assays. The experimental results revealed that knockdown of TTN-AS1 obviously inhibited GC cell proliferation, induced cell apoptosis and impaired cell migration and invasion. In mechanism, TTN-AS1 was located in the cytoplasm of GC cells, indicating the post-transcriptional regulation of TTN-AS1 on gene expression. Bioinformatics analysis revealed the potential binding relation between TTN-AS1 and miR-376b-3p as well as between miR-376b-3p and KLF12. Mechanism experiments such as luciferase reporter assay and RNA pull-down assay demonstrated the interaction between TTN-AS1 and miR-376b-3p as well as between miR-376b-3p and KLF12 in GC cells. At last, rescue assays certified that miR-376b-3p and KLF12 involved in TTN-AS1-mediated GC progression. Similarly, the role of TTN-AS1-miR-376b-3p-KLF12 axis in GC progression was analyzed and validated. Taken together, we concluded that TTN-AS1 might function as a novel potential therapeutic target in the treatment of gastric cancer.

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“…The normal bone marrows were used as controls. CD138 + cells were selected and purified from the bone marrow based on previous described [ 22 ]. This study was approved by the Clinical Research Ethics Committee of China-Japan Union Hospital of Jilin University.…”

Section: Methodsmentioning

confidence: 99%

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

2019

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Background: Long non-coding RNA taurine up-regulated gene 1 (TUG1) was reportedly involved in initiation and development of several cancers. However, its function and molecular mechanisms in multiple myeloma (MM) are still unclear. The present study aimed to determine the expression status, biological function, and potential mechanisms of TUG1 in the progression of MM. Materials and methods: The expression levels of TUG1 were examined in MM samples and cell lines by real-time quantitative PCR. The effects of TUG1 on MM cells proliferation and apoptosis were assessed using Cell Counting Kit-8 assay and flow cytometry respectively. MiRNAs-targeted sites in TUG1 were screened by Starbase2.0 and were identified by RNA immunoprecipitation assay combined with luciferase reporter assay. Results: The expression levels of TUG1 were markedly increased in MM samples and cell lines. Knockdown of TUG1 significantly suppressed the proliferation, induced cell cycle arrest at G1/G0 phase, and promoted apoptosis of MM cells. In exploring the regulatory mechanism, miR-29b-3p was confirmed to be a direct target of TUG1, and repression of miR-29b-3p could partially rescue the effect TUG1 knockdown on MM cell proliferation, cycle, and apoptosis. In addition, TUG1 positively modulated histone deacetylases 4 (HDAC4, a target of miR-29b-3p) expression through sponging of miR-29b-3p in MM cells. Conclusion: These findings suggested that TUG1 exerted an oncogenic role in MM by acting as a competing endogenous RNA of miR-29b-3p, and implied the potential application of TUG1 in treatment for MM.

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Long Non-Coding RNA TUG1 as a Potential Novel Biomarker for Predicting the Clinical Outcome of Cancer Patients: a Meta-Analysis

Cited by 7 publications

References 0 publications

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

LncRNA TTN-AS1 contributes to gastric cancer progression by acting as a competing endogenous RNA of miR-376b-3p

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

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