A tumor-suppressive microRNA, miR-504, inhibits cell proliferation and promotes apoptosis by targeting FOXP1 in human glioma

Cui, Run; Guan, Yanlei; Sun, Chuanqi; Chen, Ling; Bao, Yijun; Li, Guangyu; Qiu, Bo; Meng, Xin; Pang, Chao; Wang, Yunjie

doi:10.1016/j.canlet.2016.01.051

Cited by 45 publications

(40 citation statements)

References 37 publications

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“…For example, miR-208a-3p promotes gastric cancer cell proliferation via targeting PDCD4 3′-UTR (Yin et al, 2016). Meanwhile, miR-504 exerts tumor-suppressive function via targeting FOXP1 3′-UTR in glioma (Cui et al, 2016). In our study, three kinds of bioinformatics softwares indicated CCNE2 was a target of miR-370.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells’ Malignancy by Activating miR-370/CCNE2 Axis

Gong

Zheng

Liu

et al. 2017

Front. Cell. Neurosci.

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Accumulating evidence has highlighted the potential role of long non-coding RNAs (lncRNAs) as biomarkers and therapeutic targets in solid tumors. Here, we elucidated the function and possible molecular mechanisms of lncRNA KCNQ1OT1 in human glioma U87 and U251 cells. Quantitative Real-Time polymerase chain reaction (qRT-PCR) demonstrated that KCNQ1OT1 expression was up-regulated in glioma tissues and cells. Knockdown of KCNQ1OT1 exerted tumor-suppressive function in glioma cells. Moreover, a binding region was confirmed between KCNQ1OT1 and miR-370 by dual-luciferase assays. qRT-PCR showed that miR-370 was down-regulated in human glioma tissue and cells. In addition, restoration of miR-370 exerted tumor-suppressive function via inhibiting cell proliferation, migration and invasion, while promoting the apoptosis of human glioma cells. Knockdown of KCNQ1OT1 decreased the expression level of Cyclin E2 (CCNE2) by binding to miR-370. Further, miR-370 bound to CCNE2 3′UTR region and decreased the expression of CCNE2. These results provided a comprehensive analysis of KCNQ1OT1-miR-370-CCNE2 axis in human glioma cells and might provide a novel strategy for glioma treatment.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells’ Malignancy by Activating miR-370/CCNE2 Axis

Gong

Zheng

Liu

et al. 2017

Front. Cell. Neurosci.

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“…As a CTGF downstream, miR-504 is repressed by CTGF and carries out its ‘onco-miR’ function through targeting FOXP1 [135]. Cui and his colleagues identified FOXP1 as a direct target of miR-504 in glioma tumorigenesis and showed that miR-504/FOXP1 signaling significantly decreases cellular invasiveness and inhibits lymph node metastasis [136]. The biological mechanisms by which miR-504/FOXP1 signaling exerts opposing roles to tumorigenesis of different cancers need to be further elucidated.…”

Section: Fox-related Mirnasmentioning

confidence: 99%

MicroRNAs as regulators and mediators of forkhead box transcription factors function in human cancers

Zhang

Chen

et al. 2016

Oncotarget

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Evidence has shown that microRNAs are widely implicated as indispensable components of tumor suppressive and oncogenic pathways in human cancers. Thus, identification of microRNA targets and their relevant pathways will contribute to the development of microRNA-based therapeutics. The forkhead box transcription factors regulate numerous processes including cell cycle progression, metabolism, metastasis and angiogenesis, thereby facilitating tumor initiation and progression. A complex network of protein and non-coding RNAs mediates the expression and activity of forkhead box transcription factors. In this review, we summarize the current knowledge and concepts concerning the involvement of microRNAs and forkhead box transcription factors and describe the roles of microRNAs-forkhead box axis in various disease states including tumor initiation and progression. Additionally, we describe some of the technical challenges in the use of the microRNA-forkhead box signaling pathway in cancer treatment.

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“…Gliomas are the most common primary central nervous system(CNS) tumors in adults [1]. According to the newest WHO classification of tumors of CNS, gliomas were categorized into four grades (WHO Grade I to IV) on the basis of histologic criteria [2].…”

Section: Introductionmentioning

confidence: 99%

A Novel Tumor-Suppressor, CDH18, Inhibits Glioma Cell Invasiveness Via UQCRC2 and Correlates with the Prognosis of Glioma Patients

Bai

Zhan

et al. 2018

Cell Physiol Biochem

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Background/Aims: CDH18 (cadherin 18) is specifically expressed in the central nervous system and associated with various neuropsychiatric disorders. In this study, the role of CDH18 in glioma carcinogenesis and progression was investigated. Methods: The expression of CDH18 and its prognostic value in patients with gliomas were analyzed in public database and validated by real-time PCR/immunohistochemical staining (IHC) in our cohort. CCK-8 assay, transwell migration assay, wound healing assay, clonogenic assay and tumorigenicity assay were used to compare the proliferation, invasion and migration ability of glioma cells with different expressions of CDH18. iTRAQ-based quantitative proteomic analysis were used to reveal the downstream target of CDH18. Rescue experiments were conducted to further validate the relationship between UQCRC2 and CDH18. Results: The expression of CDH18 was depressed in a ladder-like pattern from normal tissues to WHO IV gliomas, and was an independent prognostic factor in TCGA (The Cancer Genome Atlas), CGGA (the Chinese glioma genome-atlas) and our glioma cohorts (n=453). Functional experiments in vitro and in vivo demonstrated that CDH18 inhibited invasion/migration, enhanced chemoresistance and suppressed tumorigenicity of glioma cells. UQCRC2 was identified as the downstream target of CDH18 by proteomic analysis. The expression of UQCRC2 was gradually absent as the WHO grades of gliomas escalated and was positively correlated with the expression of CDH18. Furthermore, in vitro assays demonstrated that down-regulation of UQCRC2 partly reversed the inhibition of invasion/migration ability and chemoresistance in CDH18 overexpressed glioma cell lines. Survival analysis demonstrated that combined CDH18/UQCRC2 biomarkers significantly influenced the prognosis of glioma patients. Conclusions: The present research demonstrated that CDH18 exerted its tumor-suppressor role via UQCRC2 in glioma cells and CDH18 might serve as a therapeutic target for treating gliomas.

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A tumor-suppressive microRNA, miR-504, inhibits cell proliferation and promotes apoptosis by targeting FOXP1 in human glioma

Cited by 45 publications

References 37 publications

RETRACTED: Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells’ Malignancy by Activating miR-370/CCNE2 Axis

RETRACTED: Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells’ Malignancy by Activating miR-370/CCNE2 Axis

MicroRNAs as regulators and mediators of forkhead box transcription factors function in human cancers

A Novel Tumor-Suppressor, CDH18, Inhibits Glioma Cell Invasiveness Via UQCRC2 and Correlates with the Prognosis of Glioma Patients

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