Expression profile analysis of microRNAs and downregulated miR-486-5p and miR-30a-5p in non-small cell lung cancer

Zhu, Jianjie; Zeng, Yuanyuan; Xu, Chun; Qin, Hualong; Li, Zhe; Shen, Dan; Liu, Zeyi; Huang, Jianan

doi:10.3892/or.2015.4141

Cited by 53 publications

(58 citation statements)

References 44 publications

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“…Notably, miR-30a-5p has been implicated in many types of human malignancies. For instance, miR-30a-5p is overexpressed in glioma (11) but significantly downregulated in lung cancer (12). Accordingly, miR-30a-5p serves different roles in different types of cancer (11,12), and its functions require full elucidation in different cancer types including HCC.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-30a-5p suppresses proliferation, invasion and tumor growth of hepatocellular cancer cells via targeting FOXA1

et al. 2017

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Abstract. Deregulation of microRNAs (miRs) has been observed in a variety of types of human cancer. Previously, miR-30a-5p has been demonstrated to exhibit a suppressive role in hepatocellular carcinoma (HCC). However, the underlying mechanism remains largely unclear. The present study aimed to elucidate the regulatory mechanism of miR-30a-5p in proliferation and invasion of HCC cells. Quantitative reverse transcription polymerase and western blotting were used to examine mRNA and protein expression of Forkhead box A1 (FOXA1). MTT and Transwell assays were performed to examine proliferation and invasion. Luciferase reporter assay was used to determine the association between miR-30a-5p and FOXA1. The data indicated that miR-30a-5p was significantly downregulated in HCC tissues compared with normal liver tissues. Furthermore, the level of miR-30a-5p was lower in HCC tissues with higher histological grade and advanced tumor stage compared with tissues with lower histological grade and tumor stage. Additionally, restoration of miR-30a-5p expression decreased the proliferation and invasion of HCC HepG2 and SMMC-7721 cells. FOXA1, a novel oncogene in HCC, was further identified as a target of miR-30a-5p. Furthermore, high expression of miR-30a-5p suppressed mRNA and protein expression of FOXA1, while overexpression of FOXA1 reversed the suppressive effect of miR-30a-5p on proliferation and invasion of HepG2 and SMMC-7721 cells. FOXA1 was markedly upregulated in HCC tissues compared with normal liver tissues, and its level was higher in HCC tissues with higher histological grade and advanced tumor stage. In addition, it was found that overexpression of miR-30a-5p significantly suppressed the tumor growth of HCC cells in nude mice. Taken together, the present study supports that miR-30a-5p inhibits the proliferation, invasion, and tumor growth of HCC cells, partly at least, by inhibition of FOXA1 expression, and therefore suggests that miR-30a-5p may serve as a potential candidate for HCC therapy.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-30a-5p suppresses proliferation, invasion and tumor growth of hepatocellular cancer cells via targeting FOXA1

et al. 2017

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“…Zhang et al suggested that miR-486-5p could be a biomarker and play a suppressor gene in NSCLC [19]. Some studies have also shown the effect of miR-486-5p on inhibition of the development and growth of NSCLC in mouse models [29, 30].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-486-5p is significantly downregulated in NSCLC [19], breast cancer [20], hepatocellular carcinoma [21], chronic kidney disease [22], spinal cord injury [23], and Duchenne muscular dystrophy (DMD) [24]. Based on this correlation, we hypothesized that miR-486-5p may play an important role in tumorigenesis and tumor development in NSCLC.…”

Section: Introductionmentioning

confidence: 99%

Direct repression of the oncogene CDK4 by the tumor suppressor miR-486-5p in non-small cell lung cancer

Shao

Shen

et al. 2016

Oncotarget

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MicroRNAs are a class of non-coding single-stranded RNA, 20-23 nucleotide in length, which can be involved in the regulation of gene expression. Through binding with 3'-untranslated regions (3'-UTR), microRNAs can cause degradation of target mRNAs or inhibition of translation, and thus regulating the expression of genes at the post-transcriptional level. In this study, we found that miR-486-5p was significantly downregulated in non-small cell lung cancer (NSCLC) tissues and cell lines, suggesting that miR-486-5p might function as a tumor suppressor in lung cancer. Additionally, we showed that CDK4, an oncogene that plays an important role in cell cycle G1/S phase progression, was directly targeted by miR-486-5p. Furthermore, our data reveals that knockdown of CDK4 by siRNA can inhibit cell proliferation, promote apoptosis, and impede cell-cycle progression. In epigenetics, the upstream promoter of miR-486-5p was strongly regulated by methylation in NSCLC. Collectively, our results suggest that miR-486-5p could not only inhibit NSCLC by downregulating the expression of CDK4, but also be as a promising and potent therapy in the near future.

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“…ANK1 is a host gene for miR-486 [162] which in turn is a source of two mature miR-486 miRNAs, namely, miR-486-3p and miR-486-5p [163]. Importantly, ANK1 hypermethylation inhibits the transcription of miR-486 [164], which may have pathogenic consequences as suppression of this miRNA has pro-inflammatory consequences and is furthermore associated with increased cellular survival and proliferation [165,166]. Furthermore, upregulation of miR-486 acts as a negative regulator of Akt (protein kinase B), mTOR and STAT3 (signal transducer and activator of transcription 3), all of which play major roles in microglial activation, proliferation and survival [167,168].…”

Section: Epigenetic Dysregulation Of Ank1 As a Source Of Microglial Pmentioning

confidence: 99%

Could Alzheimer’s Disease Originate in the Periphery and If So How So?

et al. 2018

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The classical amyloid cascade model for Alzheimer's disease (AD) has been challenged by several findings. Here, an alternative molecular neurobiological model is proposed. It is shown that the presence of the APOE ε4 allele, altered miRNA expression and epigenetic dysregulation in the promoter region and exon 1 of TREM2, as well as ANK1 hypermethylation and altered levels of histone post-translational methylation leading to increased transcription of TNFA, could variously explain increased levels of peripheral and central inflammation found in AD. In particular, as a result of increased activity of triggering receptor expressed on myeloid cells 2 (TREM-2), the presence of the apolipoprotein E4 (ApoE4) isoform, and changes in ANK1 expression, with subsequent changes in miR-486 leading to altered levels of protein kinase B (Akt), mechanistic (previously mammalian) target of rapamycin (mTOR) and signal transducer and activator of transcription 3 (STAT3), all of which play major roles in microglial activation, proliferation and survival, there is activation of microglia, leading to the subsequent (further) production of cytokines, chemokines, nitric oxide, prostaglandins, reactive oxygen species, inducible nitric oxide synthase and cyclooxygenase-2, and other mediators of inflammation and neurotoxicity. These changes are associated with the development of amyloid and tau pathology, mitochondrial dysfunction (including impaired activity of the electron transport chain, depleted basal mitochondrial potential and oxidative damage to key tricarboxylic acid enzymes), synaptic dysfunction, altered glycogen synthase kinase-3 (GSK-3) activity, mTOR activation, impairment of autophagy, compromised ubiquitin-proteasome system, iron dyshomeostasis, changes in APP translation, amyloid plaque formation, tau hyperphosphorylation and neurofibrillary tangle formation.

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Expression profile analysis of microRNAs and downregulated miR-486-5p and miR-30a-5p in non-small cell lung cancer

Cited by 53 publications

References 44 publications

MicroRNA-30a-5p suppresses proliferation, invasion and tumor growth of hepatocellular cancer cells via targeting FOXA1

MicroRNA-30a-5p suppresses proliferation, invasion and tumor growth of hepatocellular cancer cells via targeting FOXA1

Direct repression of the oncogene CDK4 by the tumor suppressor miR-486-5p in non-small cell lung cancer

Could Alzheimer’s Disease Originate in the Periphery and If So How So?

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