Long non‐coding <scp>RNA TUG</scp>1 promotes migration and invasion by acting as a ce<scp>RNA</scp> of miR‐335‐5p in osteosarcoma cells

Wang, Yong; Yang, Tao; Zhang, Zhen; Lu, Ming; Zhao, Wei; Zeng, Xiandong; Zhang, Weiguo

doi:10.1111/cas.13201

Cited by 118 publications

(102 citation statements)

References 51 publications

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“…reported that the novel long intergenic noncoding RNA upregulated in CRC (UCC) promoted CRC progression by sponging miR-143. TUG1 plays a role in the regulation of many cancer types by functioning as a ceRNA Wang et al [22,32,34,35,53]. Based on the results of our bioinformatics analysis, it was hypothesized that miR-142-3p could be negatively regulated by TUG1.…”

Section: Discussionmentioning

confidence: 79%

“…In a ceRNA model, lncRNA release or upregulate target mRNA of miRNAs by competitively binding with the same miRNAs Zhang et al [27][28][29][30][31]. TUG1 participates in the progression and development of multiple tumors by acting as a ceRNA Zhang et al [22,24,26,[32][33][34][35][36]. To determine whether TUG1 acts as a ceRNA in HCC, we applied bioinformatics analysis (http://starbase.sysu.edu.…”

Section: Tug1 Regulates Zeb1 By Competitively Binding With Mir-142-3pmentioning

confidence: 99%

“…The lncRNA taurine upregulated gene 1 (TUG1) plays a role in the progression of several human cancers by interacting with miRNAs Wang et al [22][23][24]. For example, TUG1 accelerates the malignancy of pancreatic cancer through sponging miR-382 Zhao et al [25], mediates methotrexate resistance in colorectal cancer (CRC) by interacting with miR-186 Li et al [26], acts as an oncogene in osteosarcoma by binding with miR-335 Wang et al [22], and improves gastric cancer progression through sponging miR-145-5p Ren et al [24]. Thus, this study aimed to clarify the interaction between TUG1 and miR-142-3p in HCC.…”

Section: Introductionmentioning

confidence: 99%

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lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Liu

Jin

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNA-142-3p (miR-142-3p) is dysregulated in many malignancies and may function as a tumor suppressor or oncogene in tumorigenesis and tumor development. However, few studies have investigated the clinical significance and biological function of miR-142-3p in hepatocellular carcinoma (HCC). Methods: The expression levels of taurine upregulated gene 1 (TUG1), miR-142-3p, and zinc finger E-box-binding homeobox 1 (ZEB1) were evaluated in HCC tissues and cell lines by quantitative real-time PCR. MTT and colony formation assays were used to detect cell proliferation ability, transwell assays were used to assess cell migration and invasion, and luciferase reporter assays were used to examine the interaction between the long noncoding RNA TUG1 and miR-142-3p. Tumor formation was evaluated through in vivo experiments. Results: miR-142-3p was significantly downregulated in HCC tissues, but TUG1 was upregulated in HCC tissues. Knockdown of TUG1 and upregulation of miR-142-3p inhibited cell proliferation, cell migration, cell invasion, and the epithelial-mesenchymal transition (EMT). miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulated ZEB1 was via direct binding to miR-142-3p. In vivo assays showed that TUG1 knockdown suppressed cell proliferation and the EMT in nude mice. Conclusion: The results of this study suggest that the TUG1/miR-142-3p/ ZEB1 axis contributes to the formation of malignant behaviors in HCC.

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Section: Discussionmentioning

confidence: 79%

Section: Tug1 Regulates Zeb1 By Competitively Binding With Mir-142-3pmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Liu

Jin

et al. 2018

Cell Physiol Biochem

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“…For example, it is reported that lncRNA PTENP1 functioned as a ceRNA to modulate PTEN levels by decoying miR-106b and miR-93 in gastric cancer [33]. Similarly, Wang et al found that lncRNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells [34]. In addition, lncRNA TUG1 has been revealed to stimulate human …”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer

Chang¹,

Guo²,

Zhang³

et al. 2018

Cell Physiol Biochem

102

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Background/Aims: The long noncoding RNA homeobox (HOX) transcript antisense intergenic RNA (HOTAIR) has been demonstrated to be a vital modulator in the proliferation and metastasis of ovarian cancer cells, but its potential molecular mechanism remains to be elucidated. In the current study, we aimed to uncover the biological role of lncRNA HOTAIR and its underlying regulatory mechanism in the progression and metastasis of ovarian cancer. Methods: HOTAIR expression was detected by quantitative RT-PCR (qRT-PCR) and northern blotting. The SKOV3 ovarian cancer cell line was chosen for the subsequent assays. In addition, the molecular mRNA and protein expression levels were examined by qRT-PCR and western blotting. The competitive endogenous RNA (ceRNA) mechanism was validated by bioinformatics analysis and a dual luciferase reporter gene assay. Results: HOTAIR expression was significantly higher in ovarian carcinoma tissues and cell lines than in the control counterparts. Both CCND1 and CCND2 were downstream targets of miR-206. The inhibition of HOTAIR elevated the expression of miR-206 and inhibited the expression of CCND1 and CCND2. Moreover, CCND1 and CCND2 were highly expressed in ovarian cancer tissues, and their expression was positively correlated with HOTAIR expression. Finally, the functional assays indicated that the anticancer effects of miR-206 could be rescued by the simultaneous overexpression of either CCND1 or CCND2 in ovarian cancer. Conclusion: HOTAIR enhanced CCND1 and CCND2 expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.

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“…LncRNA‐TCONS_00026907 is involved in cervical cancer progression through inhibiting miR‐143‐5p (Jin et al, ). LncRNA MALAT1 can promote metastasis and proliferation by acting as a ceRNA of miR‐144‐3p in osteosarcoma cells (Wang, Yang et al, ). LncRNA TUG1 can promote migration and invasion by sponging miR‐335‐5p in osteosarcoma cells (Wang, Zhang et al, ).…”

Section: Discussionmentioning

confidence: 99%

LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

Liu

Yuan

Sun

et al. 2018

Journal Cellular Physiology

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Osteosarcoma is recognized as a malignant tumor in the skeletal system. Long non-coding RNAs (lncRNAs) have been exhibited to play crucial roles in osteosarcoma development. Our current study focused on the biological effects and mechanism of LINC00968 in osteosarcoma pathogenesis. We observed that LINC00968 was dramatically elevated in osteosarcoma cells including U2OS, MG63, Saos-2, SW1353, and 143-B cells compared to human osteoblast cell line hFOB. Silence of LINC00968 inhibited osteosarcoma cell growth and proliferation in vitro. Reversely, overexpression of LINC00968 promoted osteosarcoma cell survival and cell colony formation ability in Saos-2 and 143-B cells. In addition, LINC00968 was able to induce osteosarcoma cell migration and invasion through up-regulating MMP-2 and MMP-9 protein levels. The phosphoinosmde-3-kinase/Protein Kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway has been reported to participate in several cancer types. Here, in our study, we found that PI3K/AKT/mTOR pathway was involved in osteosarcoma progression. Knockdown of LINC00968 inactivated PI3K/AKT/mTOR signaling pathway in vitro. Subsequently, in vivo tumor xenografts were established using 143-B cells to investigate whether LINC00968 can induce osteosarcoma development in vivo. Consistently, it was indicated that inhibition of LINC00968 significantly inhibited osteosarcoma progression in vivo. Taken these together, in our research, LINC00968 could be provided as a novel prognostic biomarker and therapeutic target in osteosarcoma diagnosis and treatment.

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Long non‐coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR‐335‐5p in osteosarcoma cells

Cited by 118 publications

References 51 publications

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer

LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling

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