miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

Shang, Chao; Hong, Yang; Guo, Yan; Liu, Yunhui; Xue, Yi‐Xue

doi:10.3892/ol.2015.3927

Cited by 31 publications

(28 citation statements)

References 22 publications

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“…The miR‐128 ASOs might accelerate the growth of SHG‐44/DDP cells by targeting JAG1. This finding was in consistency with a previous study by Palumbo et al, which stated that up‐regulation of miR‐128 inhibits the growth of tumor in xenografts through directly targeting PTEN and BMI1 and such effects would be restored with inhibition of miR‐128 . The promotion of SHG‐44/DDP cells by miR‐128 ASO may be due to the fact that enhancing DDP resistance could suppress the apoptosis and promote the proliferation conditions of SHG‐44 cells.…”

Section: Discussionsupporting

confidence: 92%

Retracted: Effect of microRNA‐128 on cisplatin resistance of glioma SHG‐44 cells by targeting JAG1

Zhang

et al. 2017

J of Cellular Biochemistry

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This current study intends to investigate the effect of microRNA-128 (miR-128) on cisplatin (DDP) resistance in glioma SHG-44 cells. SHG-44/DDP cells were transfected with miR-128 antisense oligonucleotide (ASO) and assigned into blank, resistance, NC, anti-miR-128, miR-128 mimic, si-JAG1, and anti-miR-128 + si-JAG1 groups. qRT-PCR and Western blotting were employed for determining expression of miR-128, JAG1, Bax and Bcl-2. MTT assay, Giemsa staining, and flow cytometry were applied to detect DDP resistance, cellular morphology, and cell cycle, respectively. JAG1 is targeted and negatively regulated by miR-128. In in vitro experiments, compared with the blank group, the rest groups exhibited declined miR-28 and Bax expression, lowered cell inhibition rate and apoptosis rate, but elevated JAG1 and Bcl-2 expression with cells arrested in the S phase. Compared with the resistance group, the anti-miR-128 group showed decreasedBax expression along with a lowered cell inhibition rate and apoptosis rate, but increased JAG1 and Bcl-2 expression with reduced cells arrested in the S phase; while the miR-128 mimic group showed an opposite trend; the si-JAG1 group showed decreased Bcl-2 expression and reduced cells in the S phase. In in vivo experiments, compared with the resistance group, the tumor growth rate, tumor volume, and weight as well as JAG1 expression accelerated in the anti-miR-128 group; whereas the miR-128 mimic and si-JAG1 groups exhibited an opposite trend. Our findings demonstrated that miR-128 ASO transfection might down-regulate the expression of miR-128 in SHG-44/DDP and up-regulate the DDP resistance in SHG-44/DDP cells, providing a potential treatment target for glioma.

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Section: Discussionsupporting

confidence: 92%

Retracted: Effect of microRNA‐128 on cisplatin resistance of glioma SHG‐44 cells by targeting JAG1

Zhang

et al. 2017

J of Cellular Biochemistry

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“…Targets are the genes encoding Bmi-1, E2F3a, EGFR, PDGFRA, WEE1, Msi1 and p70SK1. [135][136][137] Bmi-1 is a PcG protein with a known oncogene effect. E2F3A is a transcription factor and together with elevated levels of EGFR and PDGFRA stimulates cell proliferation.…”

Section: Ecreased Levels Of Mir-128mentioning

confidence: 99%

On the Concepts and History of Glioblastoma Multiforme - Morphology, Genetics and Epigenetics

Stoyanov¹,

Dzhenkov²

2018

Folia Medica

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Glioblastoma multiforme (GBM) is a grade IV WHO malignant tumor with astrocytic differentiation. As one of the most common clinically diagnosed central nervous system (CNS) oncological entries, there have been a wide variety of historical reports of the description and evolution of ideas regarding these tumors. The first recorded reports of gliomas were given in British scientific reports, by Berns in 1800 and in 1804 by Abernety, with the first comprehensive histomorphological description being given in 1865 by Rudolf Virchow. In 1926 Percival Bailey and Harvey Cushing gave the base for the modern classification of gliomas. Between 1934 and 1941 the most prolific researcher in glioma research was Hans-Joachim Scherer, who postulated some of the clinico-morphological aspects of GBM. With the introduction of molecular and genetic tests the true multifomity of GBM has been established, with different genotypes bearing the same histomorphological and IHC picture, as well as some of the aspects of gliomagenesis. For a GBM to develop, a specific trigger mutation needs to occur in a GBM stem cell - primary GBM, or a slow aggregation of individual mutations, without a distinct trigger mutation - secondary GBM. Knowledge of GBM has been closely related to general medical knowledge of the CNS since these malignancies were first described more than 200 years ago. Several great leaps have been made in that time, in the footsteps of both CNS and advancements in general medical knowledge.

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“…miR-128 is an intronic miRNA encoded by two distinct genes, miR-128-1 and miR-128-2, in introns of R3H domain containing 1 ( R3HDM1 ) and cyclic AMP-regulated phosphoprotein, 21 kDa ( ARPP-21 ) genes, respectively. Furthermore, miR-128 can induce glioma cell death and inhibit migration through targeting RhoE [9], EphB2 [10], p70S6K1 [11], Bmi-1 [12], and E2F3a [13]. Serum miR-128 levels can be used as a sensitive and specific biomarker of gliomas [14].…”

Section: Introductionmentioning

confidence: 99%

The Inhibition of microRNA-128 on IGF-1-Activating mTOR Signaling Involves in Temozolomide-Induced Glioma Cell Apoptotic Death

et al. 2016

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Temozolomide (TMZ), an alkylating agent of the imidazotetrazine series, is a first-line chemotherapeutic drug used in the clinical therapy of glioblastoma multiforme, the most common and high-grade primary glioma in adults. Micro (mi)RNAs, which are small noncoding RNAs, post-transcriptionally regulate gene expressions and are involved in gliomagenesis. However, no studies have reported relationships between TMZ and miRNA gene regulation. We investigated TMZ-mediated miRNA profiles and its molecular mechanisms underlying the induction of glioma cell death. By performing miRNA microarray and bioinformatics analyses, we observed that expression of 248 miRNAs was altered, including five significantly upregulated and 17 significantly downregulated miRNAs, in TMZ-treated U87MG cells. miR-128 expression levels were lower in different glioma cells and strongly associated with poor survival. TMZ treatment significantly upregulated miR-128 expression. TMZ significantly enhanced miR-128-1 promoter activity and transcriptionally regulated miR-128 levels through c-Jun N-terminal kinase 2/c-Jun pathways. The overexpression and knockdown of miR-128 expression significantly affected TMZ-mediated cell viability and apoptosis-related protein expression. Furthermore, the overexpression of miR-128 alone enhanced apoptotic death of glioma cells through caspase-3/9 activation, poly(ADP ribose) polymerase degradation, reactive oxygen species generation, mitochondrial membrane potential loss, and non-protective autophagy formation. Finally, we identified that key members in mammalian target of rapamycin (mTOR) signaling including mTOR, rapamycin-insensitive companion of mTOR, insulin-like growth factor 1, and PIK3R1, but not PDK1, were direct target genes of miR-128. TMZ inhibited mTOR signaling through miR-128 regulation. These results indicate that miR-128-inhibited mTOR signaling is involved in TMZ-mediated cytotoxicity. Our findings may provide a better understanding of cytotoxic mechanisms of TMZ involved in glioblastoma development.

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miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

Cited by 31 publications

References 22 publications

Retracted: Effect of microRNA‐128 on cisplatin resistance of glioma SHG‐44 cells by targeting JAG1

Retracted: Effect of microRNA‐128 on cisplatin resistance of glioma SHG‐44 cells by targeting JAG1

On the Concepts and History of Glioblastoma Multiforme - Morphology, Genetics and Epigenetics

The Inhibition of microRNA-128 on IGF-1-Activating mTOR Signaling Involves in Temozolomide-Induced Glioma Cell Apoptotic Death

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