miR-603 promotes glioma cell growth via Wnt/β-catenin pathway by inhibiting WIF1 and CTNNBIP1

Guo, Mian; Zhang, Xiaoming; Wang, Guangzhi; Sun, Jing; Jiang, Zhenfeng; Khadarian, Kevork; Yu, Shan; Zhao, Yan; Xie, Chuncheng; Zhang, Kelvin; Zhu, Minwei; Shen, Hong; Lin, Zhiguo; Jiang, Chuanlu; Shen, Jia; Zheng, Yongri

doi:10.1016/j.canlet.2015.02.003

Cited by 62 publications

(50 citation statements)

References 41 publications

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“…As reported, p53 may also serve an important function in the occurrence and development of brain glioma (30). Previous studies have reported that p53 is involved in cell cycle arrest, promotion of apoptosis and maintenance of genomic stability (2,3,8,25). The present study revealed that TUG1 may promote cell apoptosis and induce cell cycle arrest, and downregulating TUG1 may function as a p53 downstream effector.…”

Section: Discussionsupporting

confidence: 62%

“…Previous studies (2,6-7) have demonstrated that the mutation of tumor protein p53, retinoblastoma protein and cyclin-dependent kinase inhibitor 2A are involved in the development of glioma; however, the etiology and pathogenesis of glioma remain unclear. Previous studies (3,5,16) have indicated that miRNAs regulate the expression of target mRNAs, which can have an effect on tumor behaviors, particularly glioma. Over the past few years, a number of lncRNAs have been identified, including HOTAIR, imprinted maternally expression transcript (H19), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and maternally expressed 3 (MEG3) (16).…”

Section: Discussionmentioning

confidence: 99%

“…The non-coding RNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), have been demonstrated to serve pivotal functions in the cancer-associated gene regulatory system (3). miRNAs may influence the growth, (3) invasion (4) and apoptosis (5) of glioma by binding with target mRNA sequences.…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of the long non-coding RNA taurine-upregulated gene 1 inhibits glioma cell proliferation and invasion and promotes apoptosis

et al. 2018

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Abstract. Expression of the long non-coding RNA taurine-upregulated gene 1 (TUG1) is associated with various aggressive tumors. The present study aimed to investigate the biological function of TUG1 in regulating apoptosis, proliferation, invasion and cell cycle distribution in human glioma U251 cells. Lentivirus-mediated TUG1-specific microRNA was transfected into U251 cells to abrogate the expression of TUG1. Flow cytometry analysis was used to examine the cell cycle distribution and apoptosis of U251 cells. Cellular proliferation was examined using Cell Counting Kit-8 (CCK-8) assays and invasion was examined by Transwell assays. The apoptotic rate of cells in the TUG1-knockdown group was significantly higher than in the negative control (NC) group (11.58 vs. 9.14%, P<0.01). CCK-8 assay data demonstrated that the proliferative ability of cells within the TUG1-knockdown group was lower compared with that of the NC group. A Transwell invasion assay was performed, which revealed that the number of invaded cells from the TUG1-knockdown group was the less compared with that of the NC group. In addition, the G 0 /G 1 phase population was significantly increased within the treated group (44.85 vs. 38.45%, P<0.01), as measured by flow cytometry. The present study demonstrated that the downregulation of TUG1 may inhibit proliferation and invasion, and promote glioma U251 cell apoptosis. In addition, knockdown of TUG1 may have an effect on cell cycle arrest.The data presented in the current study indicated that TUG1 may be a novel therapeutic target for glioma.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

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Downregulation of the long non-coding RNA taurine-upregulated gene 1 inhibits glioma cell proliferation and invasion and promotes apoptosis

et al. 2018

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“…MiR-106b-5p is located to human chromosome 7q21 and transcribed from the miR-106b-25 cluster [17, 19]. To date, a number of experiments have been designed to explore the role of miR-106b-5p in the development of various cancers [15, 16]. Over-expression of miR-106b-5p in hepatocellular carcinoma promoted cell migration and metastasis by activating epithelial-mesenchymal transition [39].…”

Section: Discussionmentioning

confidence: 99%

MiR-106b-5p Promotes Proliferation and Inhibits Apoptosis by Regulating BTG3 in Non-Small Cell Lung Cancer

Wei

Pan

Yao

et al. 2017

Cell Physiol Biochem

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Background/Aims: MicroRNAs have been validated to play a crucial role in tumorigenesis of non-small cell lung cancer (NSCLC). Although miR-106b-5p has been reported to play a vital role in various malignancies the physiological function of miR-106b-5p in NSCLC still remain unknown. In this study, we investigated the role of miR-106b-5p in NSCLC. Methods: Quantitative real-time polymerase chain reaction was conducted to estimate the expression of miR-106b-5p and BTG3 in both NSCLC tissues and cell lines. The effects of miR-106b-5p on proliferation were determined in vitro using CCK-8 proliferation assays, 5-ethynyl-2’-deoxyuridine (EdU) incorporation, colony formation assays and cell-cycle assays and the in vivo effects were evaluated by a mouse tumorigenicity model. Cell apoptosis and cell cycle was investigated by flow cytometric analysis in vitro. The molecular mechanism underlying the relevance between miR-106b-5p and BTG3 was confirmed by luciferase assay and western blot. Results: In current study, we found a relatively higher miR-106b-5p and lower BTG3 expression in NSCLC specimens and cell lines. BTG3 was verified as a direct target of miR-106b-5p by luciferase assay. In vitro, over-expression of miR-106b-5p promoted proliferation and inhibited apoptosis by down-regulating BTG3 expression. In vivo, miR-106b-5p promoted xenograft tumor formation. Conclusion: Our findings revealed for the first time that miR-106b-5p plays a tumorigenesis role in NSCLC progression by down-regulating BTG3 expression, which may lead to a novel insight to the potential biomarker and novel therapeutic strategies for NSCLC patients.

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“…DAPI was used for nuclear staining. The number of BrdU positive cells was counted in three random microscopic fields using NIH Image J software [25].…”

mentioning

confidence: 99%

MiR-142-3p Suppresses SOCS6 Expression and Promotes Cell Proliferation in Nasopharyngeal Carcinoma

Zhou

et al. 2015

Cell Physiol Biochem

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Background/Aims: An increasing number of studies show that microRNAs (miRNAs) play crucial roles in nasopharyngeal carcinoma (NPC) tumorigenesis. The aim of our study was to investigate the biological roles and mechanisms of miR-142-3p in NPC. Methods: miR-142-3p expression was examined in NPC specimens and nasopharyngitis biopsy samples by quantitative real-time PCR. The biological functions of miR-142-3p were studied using a series of in vitro and in vivo approaches. Results: miR-142-3p is over-expressed in NPC tissues and cell lines. Knockdown of miR-142-3p significantly inhibited cell proliferation and cell cycle progression in vitro, and suppressed tumor growth in a mouse model. Suppressor of cytokine signaling 6 (SOCS6) was identified as a direct target of miR-142-3p, and miR-142-3p down-regulated the expression of SOCS6 by directly binding to its 3′untranslated region (UTR). Knockdown of SOCS6 abrogated the effects of miR-142-3p down-regulation. Conclusion: These findings indicate that miR-142-3p regulates NPC development by downregulating SOCS6 expression and suggest that modulation of miR-142-3p expression could be a therapeutic strategy for NPC.

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miR-603 promotes glioma cell growth via Wnt/β-catenin pathway by inhibiting WIF1 and CTNNBIP1

Cited by 62 publications

References 41 publications

Downregulation of the long non-coding RNA taurine-upregulated gene 1 inhibits glioma cell proliferation and invasion and promotes apoptosis

Downregulation of the long non-coding RNA taurine-upregulated gene 1 inhibits glioma cell proliferation and invasion and promotes apoptosis

MiR-106b-5p Promotes Proliferation and Inhibits Apoptosis by Regulating BTG3 in Non-Small Cell Lung Cancer

MiR-142-3p Suppresses SOCS6 Expression and Promotes Cell Proliferation in Nasopharyngeal Carcinoma

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