Long non-coding RNA TUG1 promotes cervical cancer progression by regulating the miR-138-5p-SIRT1 axis

Zhu, Jie; Shi, Huirong; Liu, Huina; Wang, Xiaojuan; Li, Fengmei

doi:10.18632/oncotarget.18224

Cited by 101 publications

(81 citation statements)

References 26 publications

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“…An increasing amount of research has revealed that lncRNAs can act as ceRNAs to competitively bind to the miRNAs response elements (MRE) to regulated miRNAs functions [27]. Li et al reported that TUG1 could act as ceRNAs to regulate SIRT1 expression by sponging miR-138-5p in cervical cancer [28]. In the current study we found that MALAT1 is a target of miR-30a-5p by computational analysis, luciferase reporter assays, and RT-PCR.…”

Section: Discussionsupporting

confidence: 57%

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

Pan

Tong

Cui

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hepatocellular carcinoma (HCC) has a high morbidity as well as mortality and is believed to be one of the most prevalent cancers worldwide. The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in numerous cancers, including HCC. This study aimed to explore the role of MALAT1 in HCC progression. Methods: The expression levels of MALAT1 and Vimentin in HCC tissues and relative pair-matched adjacent normal liver tissues were analyzed by RT-PCR, and immunohistochemistry. Using bioinformatics analysis and dual-luciferase assay, we examined the correlation between MALAT1 and miR-30a-5p. Dual-luciferase assay and western blotting suggested that Vimentin was a target of miR-30a-5p. A wound healing assay and transwell assays were employed to determine the effect of MALAT1 and miR-30a-5p on cell migration and invasion in HCC. Results: Our data demonstrated that the levels of MALAT1 and Vimentin were upregulated in HCC tissues and that miR-30a-5p was a direct target of MALAT1. Silenced MALAT1 and overexpressed miR-30a-5p each inhibited cell migration and invasion. Additionally, dual-luciferase assay and western blotting demonstrated that MALAT1 could competitively sponge miR-30a-5p and thereby regulate Vimentin. Conclusion: Our data suggest that MALAT1 acts as an oncogenic lncRNA that promotes HCC migration and invasion. Therefore, the MALAT1-miR-30a-5p-Vimentin axis is a potential therapeutic target and molecular biomarker in HCC.

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Section: Discussionsupporting

confidence: 57%

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

Pan

Tong

Cui

et al. 2018

Cell Physiol Biochem

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“…can act as a ceRNA to elevate epigallocatechin gallate (EGCG)triggered CTR1 expression through sponging hsa-mir-98-5p (Jiang, Wu, Wang, Huang, & Feng, 2016 (Zhu, Shi, Liu, Wang, & Li, 2017). HOTAIR can activate cervical cancer progression by inhibiting miR-326 (X.…”

Section: Discussionmentioning

confidence: 99%

Involvement of NEAT1/miR‐133a axis in promoting cervical cancer progression via targeting SOX4

Yuan

Zhou

et al. 2019

Journal Cellular Physiology

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NEAT1 is an important tumor oncogenic gene in various tumors. Nevertheless, its involvement remains poorly studied in cervical cancer. Our study explored the functional mechanism of NEAT1 in cervical cancer. NEAT1 level in several cervical cancer cells was quantified and we found NEAT1 was greatly upregulated in vitro. NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis. For another, microRNA (miR)‐133a was downregulated in cervical cancer cells and NEAT1 negatively modulated miR‐133a expression. Subsequently, we validated that miR‐133a functioned as a potential target of NEAT1. Meanwhile, SOX4 is abnormally expressed in various cancers. SOX4 was able to act as a downstream target of miR‐133a and silencing of SOX4 can restrain cervical cancer progression. In addition, in vivo assays were conducted to prove the role of NEAT1/miR‐133a/SOX4 axis in cervical cancer. These findings implied that NEAT1 served as a competing endogenous RNA to sponge miR‐133a and regulate SOX4 in cervical cancer pathogenesis. To sum up, it was implied that NEAT1/miR‐133a/SOX4 axis was involved in cervical cancer development.

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“…Latterly, taurine upregulated gene 1 (TUG1) expression was proved to be enormously elevated in most cancers, for instance prostate cancer [11], breast cancer [12], endometrial cancer [13] and cervical cancer [14]. More than that, TUG1 was aberrantly aggrandized in HCC tissues, and it could promote cell growth and tumor formation by targeting KLF2 [15].…”

Section: Introductionmentioning

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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Long non-coding RNA TUG1 promotes cervical cancer progression by regulating the miR-138-5p-SIRT1 axis

Cited by 101 publications

References 26 publications

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

Involvement of NEAT1/miR‐133a axis in promoting cervical cancer progression via targeting SOX4

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

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