Mir-139-5p inhibits glioma cell proliferation and progression by targeting GABRA1

Wang, Lei; Liu, Yan; Yu, Zutao; Gong, Jianwu; Deng, Zhiyong; Ren, Nianjun; Zhong, Zhe; Cai, Haidong; Tang, Zhi; Cheng, Haofeng; Chen, Shuai; He, Zhengwen

doi:10.1186/s12967-021-02880-9

Cited by 26 publications

(21 citation statements)

References 33 publications

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“…we found some miRNAs acted as anti-oncogene in glioma patients (3). In a subsequent study, we have validated that miRNA-139-5p, miRNA-138-5p and miRNA-338-3p were anti-tumor factors (3)(4)(5). Another miRNA, identi ed in this study, is miRNA-383-5p, which could also be a potential therapeutic target and prognosis biomarker in glioma.…”

Section: Introductionsupporting

confidence: 62%

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Mirna-383-5p functions as an anti-oncogene in glioma through the Akt/mTOR signal pathway by targeting VEGFA

Liu

Wang

Tang

et al. 2022

Preprint

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Background Previously, we screened a series of differentially expressed miRNAs and mRNA in glioma though bioinformatics analyses which included miRNA-383-5p and vascular endothelial growth factor A(VEGFA). This work aims to investigate the effects of miRNA-383-5p on the proliferation, migration and apoptosis of glioma cells, and the regulatory mechanism of miRNA-383-5p on the VEGFA/protein kinase B(Akt)/mechanistic target of rapamycin(mTOR) pathway. Methods Cells of U87 and U251 were collected. The expression of miRNA-383-5p was detected by real-time fluorescence quantitative PCR. Akt, mTOR VEGFA and its receptor VEGFR protein expression levels in glioma cells were detected with western blotting. The relationship between miRNA-383-5p and VEGFA was verified by dual-luciferase reporter gene assay. CCK-8, Transwell and flow cytometry assays were used to detect cell proliferation, invasion and apoptosis, respectively. Results Our results indicated that overexpression of miRNA-383-5p inhibited cell proliferation, migration, and invasion and promoted apoptosis in glioma cell lines. VEGFA was identified as a target of miRNA-383-5p, and overexpression of miRNA-383-5p significantly suppressed the levels of VEGFA and Akt/mTOR signaling pathway. Overexpression of VEGFA can reverse the inhibitory effect of miRNA-383-5p and reactivate the Akt/mTOR signaling pathway. Conclution Our results suggest that miRNA-383-5p inhibits the proliferation and migration of glioma cells by regulating the VEGFA/akt/mTOR pathway.

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Section: Introductionsupporting

confidence: 62%

“…In previous studies, we identi ed nine glioma-associated miRNAs though bioinformatics tools. we found some miRNAs acted as anti-oncogene in glioma patients (3). In a subsequent study, we have validated that miRNA-139-5p, miRNA-138-5p and miRNA-338-3p were anti-tumor factors (3)(4)(5).…”

Section: Introductionmentioning

confidence: 54%

Mirna-383-5p functions as an anti-oncogene in glioma through the Akt/mTOR signal pathway by targeting VEGFA

Liu

Wang

Tang

et al. 2022

Preprint

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“…It has been shown that overexpression of miR-139-5p in vitro leads to the inhibition of cell proliferation, migration and invasion of glioma by targeting gamma-aminobutyric acid A receptor alpha 1 (GABRA1). Moreover, a correlation was found between the level of this miRNA, the probability of survival and the World Health Organization grade [ 71 ]. MiR-148a-3p is considered to be a tumor suppressor that is significantly reduced in several types of cancer, such as ovarian cancer, and gastric cancer [ 72 , 73 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA and mRNA Expression Changes in Glioblastoma Cells Cultivated under Conditions of Neurosphere Formation

Дымова

Vasileva

Kuligina

et al. 2022

CIMB

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Glioblastoma multiforme (GBM) is one of the most highly metastatic cancers. The study of the pathogenesis of GBM, as well as the development of targeted oncolytic drugs, require the use of actual cell models, in particular, the use of 3D cultures or neurospheres (NS). During the formation of NS, the adaptive molecular landscape of the transcriptome, which includes various regulatory RNAs, changes. The aim of this study was to reveal changes in the expression of microRNAs (miRNAs) and their target mRNAs in GBM cells under conditions of NS formation. Neurospheres were obtained from both immortalized U87 MG and patient-derived BR3 GBM cell cultures. Next generation sequencing analysis of small and long RNAs of adherent and NS cultures of GBM cells was carried out. It was found that the formation of NS proceeds with an increase in the level of seven and a decrease in the level of 11 miRNAs common to U87 MG and BR3, as well as an increase in the level of 38 and a decrease in the level of 12 mRNA/lncRNA. Upregulation of miRNAs hsa-miR: -139-5p; -148a-3p; -192-5p; -218-5p; -34a-5p; and -381-3p are accompanied by decreased levels of their target mRNAs: RTN4, FLNA, SH3BP4, DNPEP, ETS2, MICALL1, and GREM1. Downregulation of hsa-miR: -130b-5p, -25-5p, -335-3p and -339-5p occurs with increased levels of mRNA-targets BDKRB2, SPRY4, ERRFI1 and TGM2. The involvement of SPRY4, ERRFI1, and MICALL1 mRNAs in the regulation of EGFR/FGFR signaling highlights the role of hsa-miR: -130b-5p, -25-5p, -335-3p, and -34a-5p not only in the formation of NS, but also in the regulation of malignant growth and invasion of GBM. Our data provide the basis for the development of new approaches to the diagnosis and treatment of GBM.

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“…MicroRNAs (miRNAs), small non-coding RNAs, are abundant classes of post-transcriptional regulators with the length of 20–24 nucleotides that are involved in the control of a broad range of cellular activities, such as cell proliferation [ 22 ], differentiation [ 23 ], apoptosis [ 24 ], and metabolism [ 25 ], and play a role in the replication and propagation of viruses [ 26 , 27 ]. The nucleotides 2–7 of the miRNA 5′ end, which is called the seed-sequence, usually target the 3′ untranslated region (3′-UTR), 5′ untranslated region (5′-UTR), or the coding sequence (CDS) of mRNAs either fully or partially to degrade mRNA or inhibit translation [ 28 , 29 , 30 ].…”

Section: Introductionmentioning

confidence: 99%

Gga-miR-30c-5p Enhances Apoptosis in Fowl Adenovirus Serotype 4-Infected Leghorn Male Hepatocellular Cells and Facilitates Viral Replication through Myeloid Cell Leukemia-1

Haiyilati

Zhou

et al. 2022

Viruses

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Fowl adenovirus serotype 4 (FAdV-4) is the primary causative agent responsible for the hepatitis-hydropericardium syndrome (HHS) in chickens, leading to considerable economic losses to stakeholders. Although the pathogenesis of FAdV-4 infection has gained attention, the underlying molecular mechanism is still unknown. Here, we showed that the ectopic expression of gga-miR-30c-5p in leghorn male hepatocellular (LMH) cells enhanced apoptosis in FAdV-4-infected LMH cells by directly targeting the myeloid cell leukemia-1 (Mcl-1), facilitating viral replication. On the contrary, the inhibition of endogenous gga-miR-30c-5p markedly suppressed apoptosis and viral replication in LMH cells. Importantly, the overexpression of Mcl-1 inhibited gga-miR-30c-5p or FAdV-4-induced apoptosis in LMH cells, reducing FAdV-4 replication, while the knockdown of Mcl-1 by RNAi enhanced apoptosis in LMH cells. Furthermore, transfection of LMH cells with gga-miR-30c-5p mimics enhanced FAdV-4-induced apoptosis associated with increased cytochrome c release and caspase-3 activation. Thus, gga-miR-30c-5p enhances FAdV-4-induced apoptosis by directly targeting Mcl-1, a cellular anti-apoptotic protein, facilitating FAdV-4 replication in host cells. These findings could help to unravel the mechanism of how a host responds against FAdV-4 infection at an RNA level.

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Mir-139-5p inhibits glioma cell proliferation and progression by targeting GABRA1

Cited by 26 publications

References 33 publications

Mirna-383-5p functions as an anti-oncogene in glioma through the Akt/mTOR signal pathway by targeting VEGFA

Mirna-383-5p functions as an anti-oncogene in glioma through the Akt/mTOR signal pathway by targeting VEGFA

MicroRNA and mRNA Expression Changes in Glioblastoma Cells Cultivated under Conditions of Neurosphere Formation

Gga-miR-30c-5p Enhances Apoptosis in Fowl Adenovirus Serotype 4-Infected Leghorn Male Hepatocellular Cells and Facilitates Viral Replication through Myeloid Cell Leukemia-1

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