LncRNA TUG1 acts as a tumor suppressor in human glioma by promoting cell apoptosis

Li, Jun; Zhang, Meng; An, Gang; Ma, Qing

doi:10.1177/1535370215622708

Cited by 172 publications

(161 citation statements)

References 22 publications

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“…However, Zhang et al [10] found that TUG1 was generally downregulated in NSCLC, and low TUG1 expression was associated with advanced TNM stage, larger tumor size, as well as poorer OS. In a most recent study [16], Li et al found that TUG1 functions as a tumor suppressor in glioma by activating caspase-3 and caspase-9-mediated intrinsic pathways and inhibiting Bcl-2-mediated anti-apoptotic pathways. These findings indicate that the expression pattern of lncRNAs may feature higher tissue specificity in comparison with that of protein-coding genes [23,24].…”

Section: Discussionmentioning

confidence: 98%

“…TUG1 was recently confirmed to be upregulated in colorectal cancer [10], hepatocellular carcinoma [13], urothelial carcinoma of the bladder [14], and osteosarcoma [15] and thus facilitates the proliferation of tumor cells. By contrast, TUG1 expression has been reported to be downregulated in non-small cell lung cancer (NSCLC) and glioma [16,17], and thus, it may function as a tumor suppressor in some types of cancer. However, the expression pattern and function of TUG1 in ESCC have rarely been reported.…”

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confidence: 87%

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High TUG1 expression is associated with chemotherapy resistance and poor prognosis in esophageal squamous cell carcinoma

Jiang

Wang

et al. 2016

Cancer Chemother Pharmacol

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Section: Discussionmentioning

confidence: 98%

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confidence: 87%

High TUG1 expression is associated with chemotherapy resistance and poor prognosis in esophageal squamous cell carcinoma

Jiang

Wang

et al. 2016

Cancer Chemother Pharmacol

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“…LncRNA taurine upregulated gene 1 ( TUG1 ) was initially identified as an essential gene for retinal development in the developing mouse eye [8]. Subsequent research revealed that TUG1 was abnormally regulated in tumorigenesis, either as a potential tumor suppressor or as an oncogene [910]. However, the role of TUG1 in breast cancer is still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

LncRNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells

Zhao

Ren

2016

J Breast Cancer

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PurposeThis study was designed to investigate the role of taurine-upregulated gene 1 (TUG1) in MCF-7 breast cancer cells and the molecular mechanism involved in the regulation of microRNA-9 (miR-9).MethodsThe expression of TUG1 in breast cancer tissues and cells was evaluated using quantitative reverse transcription polymerase chain reaction. Cell viability was examined using a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay; cell cycle progression and apoptosis were analyzed using flow cytometry. A dual luciferase reporter assay was used to detect the relationship between TUG1 and miR-9. The expression of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was measured by western blot.ResultsHigher expression of TUG1 was observed in breast cancer tissues and cell lines than in the corresponding controls. TUG1 knockdown reduced proliferation, suppressed cell cycle progression, and promoted apoptosis of MCF-7 cells. The dual luciferase reporter assay showed that TUG1 could negatively regulate the expression of miR-9. MiR-9 inhibition abrogated the effect of TUG1 knockdown on the proliferation, cell cycle progression, and apoptosis of MCF-7 cells. TUG1 positively regulated the expression of MTHFD2 in breast cancer cells.ConclusionTUG1 knockdown was significantly associated with decreased cell proliferation and it promoted apoptosis of breast cancer cells through the regulation of miR-9.

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“…Moreover, radiotherapy treatment for spinal cord glioma is associated with worsened outcomes [6]. Interestingly, one study provides new insight for understanding the function of the long non-coding RNA taurine up-regulated gene 1 (lncRNA TUG1) in cancer biology, with the potential of TUG1 overexpression in glioma therapy [7].…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-κB Signaling Pathway

Han

Wen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Spinal cord glioma is a highly aggressive malignancy that commonly results in high mortality due to metastasis, high recurrence and limited treatment regimens. This study aims to elucidate the effects of long non-coding RNA LINC01260 (LINC01260) on the proliferation, migration and invasion of spinal cord glioma cells by targeting Caspase recruitment domain family, member 11 (CARD11) via nuclear factor kappa B (NF-κB) signaling. Methods: The Multi Experiment Matrix (MEM) website was used for target gene prediction, and the DAVID database was used for analysis of the relationship between CARD11 and the NF-κB pathway. In total, 60 cases of glioma tissues and adjacent normal tissues were collected. Human U251 glioma cells were grouped into blank, negative control (NC), LINC01260 vector, CARD11 vector, siRNA-LINC01260, siRNA-CARD11, LINC01260 vector + CARD11 vector and LINC01260 + siRNA-CARD11 groups. A dual-luciferase reporter assay was conducted to verify the target relationship between LINC01260 and CARD11. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were employed to assess expression of LINC01260, E-cadherin, p53, CARD11, Ki67, N-cadherin, matrix metalloproteinase (MMP)-9, NF-κBp65 and NF-κBp50. MTT, flow cytometry, wound-healing and Transwell assays were performed to examine cell viability, the cell cycle, apoptosis, invasion and migration. Tumor growth was assessed through xenografts in nude mice. Results: CARD11 was confirmed to be a target gene of LINC01260 and was found to be involved in regulating the NF-κB pathway. Compared with adjacent normal tissues, glioma tissues showed reduced expression of LINC01260 and elevated expression of CARD11 and genes related to apoptosis, invasion and migration; activation of NF-κB signaling was also observed. In contrast to the blank and NC groups, an elevated number of cells arrested in G1 phase, increased apoptosis and reduced cell proliferation, invasion and number of cells arrested in S and G2 phases, as well as tumor growth were found for the LINC01260 vector and siRNA-CARD11 groups. Conclusions: Our findings demonstrate that overexpression of LINC01260 inhibits spinal cord glioma cell proliferation, migration and invasion by targeting CARD11 via NF-κB signaling suppression.

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LncRNA TUG1 acts as a tumor suppressor in human glioma by promoting cell apoptosis

Cited by 172 publications

References 22 publications

High TUG1 expression is associated with chemotherapy resistance and poor prognosis in esophageal squamous cell carcinoma

High TUG1 expression is associated with chemotherapy resistance and poor prognosis in esophageal squamous cell carcinoma

LncRNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells

Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-κB Signaling Pathway

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