MicroRNA-27b inhibits Spry2 expression and promotes cell invasion in glioma U251 cells

Liu, Chenghui; Liang, Shi-xing; Xiao, Shengnan; Qi-ming, Lin; Xu, Chen; Wu, Yi; Fu, Jianhua

doi:10.3892/ol.2015.2865

Cited by 23 publications

(21 citation statements)

References 21 publications

(28 reference statements)

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“…It has been reported that overexpression of microRNA-155 predicts poor prognosis in glioma patients [13]. miR-27b may promote glioma cell invasion through direct inhibition of Spry2 expression [14]. In the current study, we provide the first demonstration that miR-508-5p expression is down-regulated in a human glioma tissues and cell lines.…”

Section: Neurochem Resmentioning

confidence: 84%

MiR-508-5p Inhibits the Progression of Glioma by Targeting Glycoprotein Non-metastatic Melanoma B

Bao

Wang

et al. 2016

Neurochem Res

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Glioma is a severe and highly lethal brain cancer, a malignancy largely stemming from growing in a relatively restrained area of the brain. Hence, the understanding of the molecular regulation of the growth of glioma is critical for improving its treatment. MicroRNA has become a hotspot in research on diseases, especially in the initiation and progression of different types of cancer. However, the molecular function and mechanisms of miR-508-5p in gliomagenesis are still unclear. The aim of this study was to investigate miR-508-5p expression in glioma and determine its effects on proliferation. miR-508-5p expression levels, both in glioma cell lines and in tissue, were significantly lower than in a normal human astrocyte cell line or adjacent tissues. Cell growth was analyzed using a MTT assay and over-expression of miR-508-5p was found to decrease glioma cell growth. Moreover, a bioinformatic analysis was performed, showing that glycoprotein non-metastatic melanoma B (GPNMB) was a direct target for miR-508-5p in glioma cells. Furthermore, in vivo treatment with miR-508-5p reduced GPNMB protein levels in the tumor. Additionally, overexpression of GPNMB without 3'-UTR partially reversed the cell growth arrest induced by miR-508-5p over-expression in glioma cells. In conclusion, these results indicate that increased expression of miR-508-5p might be related to glioma progression, indicating a potential role of miR-508-5p for clinical therapy.

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Section: Neurochem Resmentioning

confidence: 84%

MiR-508-5p Inhibits the Progression of Glioma by Targeting Glycoprotein Non-metastatic Melanoma B

Bao

Wang

et al. 2016

Neurochem Res

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“…Sprouty homolog 2 (SPRY2) is a member of the sprouty family and inhibits the activity of receptor tyrosine kinase signaling, which is required for the growth factor-stimulated translocation of the protein to membrane ruffles ( 17 , 18 ). Previous studies have indicated that SPRY2 serves a suppressive role in different human cancer types ( 19 – 21 ); however, the regulatory mechanism underlying SPRY2 expression in gastric cancer remains unknown.…”

Section: Introductionmentioning

confidence: 99%

microRNA‑23a promotes cell growth and metastasis in gastric cancer via targeting SPRY2‑mediated ERK signaling

Chen

She

et al. 2018

Oncol Lett

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microRNAs (miRs) serve important roles in various human cancer types. Recently, miR-23a has been indicated as an oncogene in gastric cancer, but the underlying mechanism remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction and western blot analysis was used to explore the effects of miR-23a in gastric cancer. Additionally, cell proliferation, migration and invasion were examined using an MTT assay, wound healing assay and Transwell assay, respectively. Furthermore, a luciferase reporter gene assay was used to confirm the target association. It was determined that miR-23a was significantly upregulated in gastric cancer tissues and cell lines compared with adjacent tissues, and a normal gastric epithelial cell line. Furthermore, its upregulation was significantly associated with cancer progression and poor prognosis of patients. Knockdown of miR-23a caused a notable reduction in the proliferation, migration and invasion of gastric cancer AGS cells. Sprouty homolog 2 (SPRY2) was then predicted to be target gene of miR-23a. A luciferase reporter gene assay data demonstrated that miR-23a has the ability to directly bind to the 3′-untranslational region of SPRY2 mRNA. Further investigation demonstrated that SPRY2 was significantly downregulated in gastric cancer tissues and cell lines, and the protein expression of SPRY2 was negatively regulated by miR-23a in AGS cells. Furthermore, knockdown of SPRY2 reduced the suppressive effects of miR-23a inhibition in AGS cell proliferation, migration and invasion. In addition, the activity of extracellular signal-regulated kinase (ERK) signaling was also inhibited by the miR-23a/SPRY2 knockdown in AGS cells. The present study indicated that miR-23a serves a promoting role in gastric cancer via targeting SPRY2 and downstream ERK signaling.

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“…33 MiR-27b-induced cell invasive/metastatic potential of both glioma and hepatocellular carcinoma (HCC) is directly mediated by Spry2 suppression, thereby the miR-27b/Spry2 axis may as a promising molecular target for glioma and HCC metastasis. 59,60 The up-regulated miR-27b in BRC cells alters cell migration and invasion abilities by influencing Nischarin expression and inducing PAK signaling activation. Nischarin is an α5β1 integrin binding partner, inhibiting α5 expression, along with PAK1, cofilin, and LIMK phosphorylation, and accordingly suppressing the metastatic behavior of BRC cells.…”

Section: Mir-27b Regulates Epithelial Mesenchymal Transition and Inflmentioning

confidence: 99%

Promising therapeutic role of miR-27b in tumor

Ding

Yang

et al. 2017

Tumour Biol.

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MicroRNAs are small nonprotein-encoding RNAs ranging from 18 to 25 nucleotides in size and regulate multiple biological pathways via directly targeting a variety of associated genes in cancers. MicroRNA-27b is a highly conserved MicroRNA throughout vertebrates and there are two homologs (hsa-miR-27a and hsa-miR-27b) in humans. MicroRNA27b is an intragenic microRNA located on chromosome 9q22.1 within the C9orf3 gene, clustering with miR-23b and miR-24-1 in human. As a frequently dysregulated microRNA in human cancers, microRNA-27b could function as a tumor suppressor or an oncogenic microRNA. More and more studies indicate that microRNA-27b is involved in affecting various biological processes, such as angiogenesis, proliferation, metastasis, and drug resistance, and thus may act as a promising therapeutic target in human cancers. In this review, we discuss the role of microRNA-27b in detail and offer novel insights into molecular targeting therapy for cancers.

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MicroRNA-27b inhibits Spry2 expression and promotes cell invasion in glioma U251 cells

Cited by 23 publications

References 21 publications

MiR-508-5p Inhibits the Progression of Glioma by Targeting Glycoprotein Non-metastatic Melanoma B

MiR-508-5p Inhibits the Progression of Glioma by Targeting Glycoprotein Non-metastatic Melanoma B

microRNA‑23a promotes cell growth and metastasis in gastric cancer via targeting SPRY2‑mediated ERK signaling

Promising therapeutic role of miR-27b in tumor

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