Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer

Fan, Shulin; Yang, Zhaoying; Ke, Zirui; Huang, Keke; Liu, Ning; Fang, Xuedong; Wang, Keren

doi:10.1016/j.biopha.2017.09.076

Cited by 63 publications

(39 citation statements)

References 29 publications

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“…The lncRNA BORG has been identified as a novel driver of genetic and epigenetic alterations which underlie the acquisition of metastatic and recurrent phenotypes in BRCA cells [14]. The overexpression of the lncRNA TUG1 significantly promotes cell migration and invasion, while TUG1 knockdown has the opposite effects [24]. Wang et al indicated that an elevated expression of SOX2 can activate the lncRNA PVT1, promoting BRCA tumorigenesis and progression.…”

Section: Discussionmentioning

confidence: 99%

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Feng

Wang

Liang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Next-generation sequencing (NGS) has revealed abundant long noncoding RNAs (lncRNAs) that have been characterized as critical components of cancer biology in humans. The present study aims to investigate the role of the lncRNA KCNQ1OT1 in breast cancer (BRCA) as well as the underlying molecular mechanisms and functions of KCNQ1OT1 involved in the progression of BRCA. Methods: The Cancer Genome Atlas (TCGA) and StarBase v2.0 were used to obtain the required gene data. Dual luciferase reporter gene assays were conducted to verify the relevant intermolecular target relationships. QRT-PCR and Western blot were performed to measure the expression levels of different molecules. Cell proliferation was detected by using the MTT and colony formation assays, while cell migration and invasion were examined by transwell assay. Variations in cell apoptosis and cell cycle were determined through flow cytometry. A tumor xenograft model was applied to assess tumor growth in vivo. Results: KCNQ1OT1 was found to be remarkably highly expressed in BRCA tissues and cells. KCNQ1OT1 modulated CCNE2 through sponging miR-145 in BRCA. KCNQ1OT1 promoted tumor growth in vivo by regulating miR-145/CCNE2. Conclusion: The KCNQ1OT1/miR-145/CCNE2 axis plays a critical regulatory role in BRCA, potentially giving rise to BRCA tumorigenesis and progression. These findings provide valuable evidence for improving the diagnosis and treatment of BRCA in the future.

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Section: Discussionmentioning

confidence: 99%

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Feng

Wang

Liang

et al. 2018

Cell Physiol Biochem

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“…Circular RNA may function as potential molecular markers for disease diagnosis and treatment and play an important role in the initiation and progression of human diseases, especially in tumors (Fan et al, 2017;Matjasic, Popovic, Matos, & Glavac, 2017;. In HCC, Fu et al (2017) have reported that circRNA FIGURE 6 Hsa_circ_0016788 accelerated the HCC via miR-486/CDK4 and acted as a biomarker for HCC detection.…”

Section: Hsa_circ_0016788 Accelerated the Hcc Via Mir-486/cdk4 And mentioning

confidence: 99%

Circular RNA hsa_circ_0016788 regulates hepatocellular carcinoma tumorigenesis through miR‐486/CDK4 pathway

Zheng

Tan

et al. 2018

Journal Cellular Physiology

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Recent studies have revealed that circular RNAs (circRNAs) play important roles in the tumorigenesis of human cancer, including hepatocellular carcinoma (HCC). In present study, we screen the circular RNA expression profiles in HCC tissue and investigate the molecular roles on HCC tumorigenesis. Human circRNA microarray analysis showed there were total 1,245 differently expressed circular RNAs, including 756 up-regulated circRNAs and 489 down-regulated circRNAs, in three pairs of HCC tissue and adjacent normal tissue. Hsa_circ_0016788 was identified to be up-regulated in both HCC tissue and cell lines. Loss-of-functional experiments in vivo and vitro revealed that hsa_circ_0016788 silencing inhibited the proliferation, invasion and promoted the apoptosis in vitro, and inhibited the tumor growth in vivo. Bioinformatics tools and luciferase reporter assay validated that miR-486 targeted hsa_circ_0016788 and CDK4 accompanying with negatively correlated expression, suggesting the hsa_circ_0016788/miR-486/CDK4 pathway. Receiver operating characteristic (ROC) curve showed that hsa_circ_0016788 had high diagnostic value (AUC = 0.851). In summary, results reveal the role of hsa_circ_0016788/miR-486/CDK4 in HCC tumorigenesis, providing a novel therapeutic target for HCC.

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“…Previous studies have revealed that lncRNATUG1 is involved in the development of tumors via regulation of tumor cell proliferation and migration. Furthermore, TUG1 is highly expressed in vascular endothelial cells (16,17). Yin et al (6) demonstrated that lncRNATUG1 is highly expressed in the mouse pancreas and downregulates the expression of TUG1, which subsequently affects the apoptosis and insulin secretion of pancreatic β cells, thus suggesting that lncRNATUG1 may represent a new target for the treatment of diabetes.…”

Section: Introductionmentioning

confidence: 99%

Effect of silencing lncRNATUG1 on rapamycin‑induced inhibition of endothelial cell proliferation and migration

et al. 2018

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Angiogenesis refers to the formation of new blood vessels from existing blood vessels. The proliferation and migration of endothelial cells serves a key function in this process. Previous research has demonstrated that rapamycin suppresses endothelial cell proliferation and migration, as well as angiogenesis. However, the mechanism by which rapamycin inhibits the proliferation and migration of endothelial cells remains unclear. Long noncoding RNAs (lncRNAs) serve a key function in the regulation of endothelial cell function. The aim of the current study was to investigate whether lncRNA taurine upregulated 1 (lncRNATUG1) is involved in rapamycin-induced inhibition of proliferation and migration in human umbilical vein endothelial cells (HUVECs). Reverse transcription quantitative polymerase chain reaction results indicated that the expression of lncRNATUG1 was upregulated in HUVECs that had been cultured with rapamycin. Subsequently, HUVECs were transfected with siRNAs and CCK-8 assays were performed to detect cell proliferation; additionally, flow cytometry was employed to detect cell apoptosis, and wound healing assays were performed to investigate cell migration. The results demonstrated that rapamycin suppressed the proliferation and migration of HUVECs, and promoted the apoptosis of HUVECs. In addition, rapamycin downregulated the expression of vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2 and MMP-9 in HUVECs. However, silencing of lncRNATUG1 was revealed to attenuate rapamycin-induced inhibition of cellular proliferation and migration of HUVECs, as well as upregulating the expression of VEGF, MMP2 and MMP-9. These results suggested that lncRNATUG1 regulates rapamycin-induced inhibition of endothelial cell proliferation and migration. Therefore, lncRNATUG1 may serve a key function in rapamycin-induced inhibition of endothelial cell proliferation and migration.

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Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer

Cited by 63 publications

References 29 publications

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Circular RNA hsa_circ_0016788 regulates hepatocellular carcinoma tumorigenesis through miR‐486/CDK4 pathway

Effect of silencing lncRNATUG1 on rapamycin‑induced inhibition of endothelial cell proliferation and migration

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