MicroRNA-542-3p Suppresses Tumor Cell Invasion via Targeting AKT Pathway in Human Astrocytoma

Cai, Junchao; Zhao, Jingjing; Zhang, Nu; Xu, Xiaonan; Li, Rong; Yang, Yi; Fang, Lishan; Zhang, Le; Li, Mengfeng; Wu, Jueheng; Zhang, Heng

doi:10.1074/jbc.m115.649004

Cited by 51 publications

(31 citation statements)

References 42 publications

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“…The present study showed that PI3K inhibitor (LY294002) suppressed the PI3K/AKT/survivin signal and increased the anticancer effects of miR-542-3p on apoptosis in colon cancer. Cai et al found that miR-542-3p suppressed the tumor cell invasion of human astrocytoma via targeting the AKT pathway (21).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of miR-542-3p inhibits the growth and invasion of human colon cancer cells through PI3K/AKT/survivin signaling

et al. 2017

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The present study was designed to assess the expression of microRNA-542-3p (miR-542-3p) in human colon cancer and investigate the possible molecular mechanisms underlying the effect of miR-542-3p on the growth and invasion of colon cancer cells. We found that miR-542-3p expression was downregulated in colon cancer patient tissues, compared with that observed in the control group. Silencing of miR‑542-3p expression significantly promoted cell viability and inhibited apoptosis. In addition, overexpression of miR-542-3p significantly reduced cell viability and promoted apoptosis in colon cancer cells. Meanwhile, silencing of miR-542-3p expression significantly suppressed PI3K and p-AKT and survivin protein expression, while overexpression of miR-542-3p significantly induced PI3K and p-AKT and survivin protein expression in colon cancer cells. PI3K inhibitor (LY294002) or survivin inhibitor (YM155) suppressed PI3K/AKT/survivin signaling and increased the anticancer effects of miR-542-3p on the apoptosis in colon cancer. The present study demonstrated that upregulation of miR-542-3p inhibited the growth and invasion of colon cancer cells through PI3K/AKT/survivin signaling, highlighting a novel therapeutic approach for the treatment of colon cancer.

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Section: Discussionmentioning

confidence: 99%

Upregulation of miR-542-3p inhibits the growth and invasion of human colon cancer cells through PI3K/AKT/survivin signaling

et al. 2017

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“…miR-7 directly targets PI3K [114]. The downstream Akt is targeted by miR-542-3p [115]. miR-21 indirectly regulates PI3K through targeting its antagonist PTEN [116].…”

Section: Mirna Modulates Glucose Metabolism and Glycolysis Related Simentioning

confidence: 99%

Implications of microRNA in kidney metabolic disorders

Zhou¹,

Yang²

2020

ExRNA

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The kidney requires large amount of energy to regulate the balance of fluid, electrolytes and acid-base homeostasis. Mitochondria provide indispensible energy to drive these functions. Diverse energy sources such as fatty acid and glucose are fueled for ATP production at different renal sites controlled by a fine-tuned regulation mechanism. microRNAs (miRNAs) have been implicated in the pathogenesis of various kidney diseases. Recent studies have highlighted their contributions to metabolic abnormalities. Characterization of the miRNAs in renal metabolic disorders may promote a better understanding of the molecular mechanism of these diseases and potentially serve as therapeutic targets.

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“…Furthermore, PTEN is targeted by miR-221/222, clustered in Xp11.3, which is found to be upregulated in high relative to low WHO grade glioma [ 95 , 134 ]. Additionally, the expression of the PI3K downstream effector, Akt (specifically Akt1 ), is regulated by miR-542-3p which is found to be downregulated in GBM [ 135 ]. miR-542-3p is negatively correlated with glioma WHO grade and is associated with poor prognosis [ 135 ].…”

Section: Mirna Regulation Of Rtks and Their Downstream Effector Pamentioning

confidence: 99%

MicroRNA Regulation of Glycolytic Metabolism in Glioblastoma

Alfardus

McIntyre

Smith

2017

BioMed Research International

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Glioblastoma (GBM) is the most aggressive and common malignant brain tumour in adults. A well-known hallmark of GMB and many other tumours is aerobic glycolysis. MicroRNAs (miRNAs) are a class of short nonprotein coding sequences that exert posttranscriptional controls on gene expression and represent critical regulators of aerobic glycolysis in GBM. In GBM, miRNAs regulate the expression of glycolytic genes directly and via the regulation of metabolism-associated tumour suppressors and oncogenic signalling pathways. This review aims to establish links between miRNAs expression levels, the expression of GBM glycolytic regulatory genes, and the malignant progression and prognosis of GBM. In this review, the involvement of 25 miRNAs in the regulation of glycolytic metabolism of GBM is discussed. Seven of these miRNAs have been shown to regulate glycolytic metabolism in other tumour types. Further eight miRNAs, which are differentially expressed in GBM, have also been reported to regulate glycolytic metabolism in other cancer types. Thus, these miRNAs could serve as potential glycolytic regulators in GBM but will require functional validation. As such, the characterisation of these molecular and metabolic signatures in GBM can facilitate a better understanding of the molecular pathogenesis of this disease.

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MicroRNA-542-3p Suppresses Tumor Cell Invasion via Targeting AKT Pathway in Human Astrocytoma

Cited by 51 publications

References 42 publications

Upregulation of miR-542-3p inhibits the growth and invasion of human colon cancer cells through PI3K/AKT/survivin signaling

Upregulation of miR-542-3p inhibits the growth and invasion of human colon cancer cells through PI3K/AKT/survivin signaling

Implications of microRNA in kidney metabolic disorders

MicroRNA Regulation of Glycolytic Metabolism in Glioblastoma

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