MiRNA-125a-5p inhibits glioblastoma cell proliferation and promotes cell differentiation by targeting TAZ

Yuan, Jian; Xiao, Gelei; Peng, Gang; Liu, Dingyang; Wang, Zeyou; Liao, Yixiang; Liu, Qing; Wu, Minghua; Yuan, Xianrui

doi:10.1016/j.bbrc.2014.12.078

Cited by 72 publications

(57 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It could also down-regulate P53, which consequently promotes apoptosis and enhances cell growth and invasion in multiple myeloma cells [32]. It has also been reported that miR-125a-5p is a tumor suppressor in multiple cancers through directly inhibiting the expression of numerous genes like HDAC4, E2F3, Sirtuin7, p53, and TAZ [33][34][35][36][37]. Figure 4.…”

Section: Discussionmentioning

confidence: 99%

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

Zhang¹,

Zhu²,

Li³

et al. 2015

ABBS

View full text Add to dashboard Cite

Metastasis-associated gene 1 (MTA1) is associated with cell growth, metastasis, and survival in nonsmall-cell lung cancer (NSCLC). Several previous reports have demonstrated that microRNAs affect gene expression through interaction between their seed region and the 3′-untranslated region of the target mRNA, resulting in post-transcriptional regulation. The aim of this study was to identify miRNAs that suppress malignancy in NSCLC cells by targeting MTA1. Two human NSCLC cell lines were analyzed for the expression of MTA1 by quantitative RT-PCR and western blotting after transfection with MTA1 mimics. A luciferase reporter assay was established to test the direct connection between MTA1 and its upstream miRNAs. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, 5-ethynyl-2′-deoxyuridine analysis, and colony formation assay. Cell migration and invasive capacity were evaluated by wound-healing assay and transwell assay. The miRNA/MTA1 axis was also probed by quantitative RT-PCR and western blotting in samples from eight NSCLC patients. Among the candidate miRNAs, miR-125a-3p was shown to posttranscriptionally regulate MTA1 in NSCLC cells. These data were reinforced by the luciferase reporter assay, in addition to the demonstration that MTA1 is inversely correlated with miR-125a-3p in NSCLC tissues. Furthermore, miR-125a-3p was found to inhibit NSCLC cell proliferation, migration, and invasion, through the same mechanisms of down-regulated MTA1. Our report demonstrates that miR-125a-3p inhibits the proliferation, migration, and invasion of NSCLC cells through down-regulation of MTA1, indicating the role of the miR-125a-3p/MTA1 axis in NSCLC, and may provide novel insight into the molecular mechanisms underpinning the disease and potential therapeutic targets.

show abstract

Section: Discussionmentioning

confidence: 99%

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

Zhang¹,

Zhu²,

Li³

et al. 2015

ABBS

View full text Add to dashboard Cite

show abstract

“…They are aberrantly expressed in many cancers and can exert tumor suppressive or oncogenic functions [5]. Aberrant expression of miRNAs in glioblastoma has also been reported, and many miRNAs have been shown to participate in glioblastoma tumorigenesis and/or invasion by targeting oncogenes or tumor suppressor genes, including miR-96, miR-101, MiR-125a-5p, miR-128, miR-182, miR-185, and miR-381 [6][7][8][9][10][11][12][13][14][15]. These findings indicate that miRNAs may act as another kind of important regulator in glioblastoma tumorigenesis, in addition to the protein-coding genes.…”

Section: Introductionmentioning

confidence: 96%

miR-25 promotes glioblastoma cell proliferation and invasion by directly targeting NEFL

Peng

Yuan

et al. 2015

Mol Cell Biochem

Self Cite

View full text Add to dashboard Cite

Glioblastoma multiforme (GBM) is the most malignant and common brain tumor; it is aggressive growth pattern means that GBM patients face a poor prognosis even when receiving the best available treatment modalities. In recent years, an increasing number of reports suggest that the discovery of microRNAs (miRNAs) might provide a novel therapeutic target for human cancers, including GBM. One miRNA in particular, microRNA-25 (miR-25), is overexpressed in several cancers, wherein accumulating evidence indicates that it functions as an oncogene. However, the function of miR-25 in GBM has not been totally elucidated. In this study, we demonstrated that miR-25 was significantly up-regulated in astrocytoma tissues and glioblastoma cell lines. In vitro studies further demonstrated that overexpressed miR-25 was able to promote, while its antisense oligos inhibited cell proliferation and invasion in U251 cells. Moreover, we identified neurofilament light polypeptide (NEFL) as a novel target molecule of miR-25. Also of note was the fact that NEFL was down-regulated with increased levels of miR-25 expression in human astrocytoma clinical specimens. In addition, via the mTOR signaling pathway, NEFL-siRNA could significantly attenuate the inhibitory effects of knockdown miR-25 on the proliferation and invasion of U251 cells. Overall, our results showed an important role for miR-25 in regulating NEFL expression in GBM, and suggest that miR-25 could be a potential target for GBM treatment.

show abstract

“…Overexpression of TAZ promotes CSC marker expression and sphere formation in non-CSC cancer cell populations [10,11]. More importantly, downregulation of TAZ impairs the self-renewal of breast CSCs and promoted cell differentiation in glioblastoma [10,12]. Accordingly, the Hippo pathway is considered as an important regulator in the maintenance of CSC population, and better understanding of the mechanisms that regulate Hippo pathway may provide new clues for more effective cancer therapy.…”

Section: Introductionmentioning

confidence: 97%

Upregulation of miR-130b enhances stem cell-like phenotype in glioblastoma by inactivating the Hippo signaling pathway

Zhu

Wang

Mijiti

et al. 2015

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

MiRNA-125a-5p inhibits glioblastoma cell proliferation and promotes cell differentiation by targeting TAZ

Cited by 72 publications

References 27 publications

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

miR-125a-3p targets MTA1 to suppress NSCLC cell proliferation, migration, and invasion

miR-25 promotes glioblastoma cell proliferation and invasion by directly targeting NEFL

Upregulation of miR-130b enhances stem cell-like phenotype in glioblastoma by inactivating the Hippo signaling pathway

Contact Info

Product

Resources

About