MicroRNA-30d-5p inhibits tumour cell proliferation and motility by directly targeting CCNE2 in non-small cell lung cancer

Chen, Di; Guo, Weijie; Qiu, Zhaoping; Wang, Qifeng; Li, Yan; Liang, Linhui; Liu, Li; Huang, Shenglin; Zhao, Yingjun; He, Xianghuo

doi:10.1016/j.canlet.2015.03.041

Cited by 105 publications

(109 citation statements)

References 26 publications

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“…Additionally, the clinicpathological significance of miR30d-5p in NSCLC calculated from RT-qPCR data results were consistent with the findings from the studies by Wu Y et al and Chen D et al, showing that miR-30d-5p exerted inhibitory influences on tumor progression of NSCLC [25,38]. We also appraised the prognosis-predicting and discriminatory ability of miR-30d-5p in NSCLC to achieve a comprehensive assessment of the clinico-pathological value of miR-30d-5p in NSCLC.…”

Section: Discussionsupporting

confidence: 80%

“…Current studies have reported the down-regulation of miR-30d-5p expression in NSCLC, and miR30d-5p exerts inhibitory effects on the proliferation, motility and invasion of NSCLC cells [25,35,38]. Nevertheless, the underlying molecular mechanism by which miR30d-5p regulates the tumorigenesis of NSCLC remains elusive.…”

Section: Discussionmentioning

confidence: 99%

“…In the study by Xie R et al, miR-30d-5p was reported to attenuate the migration and invasion of esophageal squamous cell carcinoma cells by regulating EZH2 expression [50]. In NSCLC, the regulatory relationship between miR-30d-5p and two target molecules, [25,38]. However, the mere revelation of two target genes of miR-30d-5p is not sufficient to interpret the molecular mechanism by which miR-30d-5p regulates the occurrence and development of NSCLC, because a single miRNA is capable of modulating the expression of hundreds of target genes.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, miR-30d-5p expression is down-regulated in NSCLC tissues, and it exerts significant suppressive effects on the tumor growth, cell cycle progression, and motility of NSCLC cells [25]. However, the precise role of miR-30d-5p in NSCLC has not yet been clarified.…”

Section: Introductionmentioning

confidence: 99%

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Expression Signature and Role of miR-30d-5p in Non-Small Cell Lung Cancer: a Comprehensive Study Based on in Silico Analysis of Public Databases and in Vitro Experiments

et al. 2018

Cell Physiol Biochem

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Background/Aims: The purpose of this study was to probe the clinico-pathological significance and the underlying mechanism of miR-30d-5p expression in non-small cell lung cancer (NSCLC). Methods: We initially examined the level of miR-30d-5p expression in NSCLC and non-cancer tissues using RT-qPCR. Then, a series of validation analyses including a meta-analysis of data from microarray chips in Gene Expression Omnibus (GEO), data mining of the cancer genome atlas (TCGA) and an integrated meta-analysis incorporating GEO microarray chips, TCGA data, in-house RT-qPCR and literature studies were performed to examine the clinico-pathological value of miR-30d-5p expression in NSCLC. In vitro experiments were further conducted to investigate the impact of miR-30d-5p on NSCLC cell growth. The molecular mechanism by which miR-30d-5p regulates the pathogenesis of NSCLC was probed through a bioinformatics analysis of its target genes. Moreover, dual luciferase reporter assay was conducted to verify the targeting regulatory relationship between miR-30d-5p and CCNE2. Results: Based on results from RT-qPCR, GEO meta-analysis, TCGA data mining and the integrated meta-analysis incorporating GEO microarray chips, TCGA data, in-house RT-qPCR and literature studies, miR-30d-5p expression was decreased in NSCLC tissues, and patients with NSCLC who presented with lower miR-30d-5p expression tended to display an advanced clinical progression. Significant pathways including the Mucin type O-glycan biosynthesis pathway, cell cycle pathway and cysteine and methionine metabolism pathway (all P< 0.05) revealed potential roles of the target genes of miR-30d-5p in the oncogenesis of NSCLC. Results from in vitro experiments indicated that miR-30d-5p could attenuate proliferation and viability of NSCLC cells. Among the 12 identified hub genes, nine genes including E2F3, CCNE2, SKP2, CDK6, TFDP1, LDHA, GOT2, DNMT3B and ST6GALNAC1 were validated by Pearson’s correlation test and the human protein atlas (HPA) database as targets of miR-30d-5p with higher probability. Specifically, dual luciferase reporter assay confirmed that CCNE2 was directly targeted by miR-30d-5p. Conclusion: In summary, miR-30d-5p expression is decreased in NSCLC, and it might play the role as tumor suppressor in NSCLC by regulating target genes.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Expression Signature and Role of miR-30d-5p in Non-Small Cell Lung Cancer: a Comprehensive Study Based on in Silico Analysis of Public Databases and in Vitro Experiments

et al. 2018

Cell Physiol Biochem

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“…In other investigations, miR-30b and miR-30c were found to inhibit sarcoma viral oncogene homolog, which affected gefitinib-induced apoptosis and the EMT of NSCLC cells (14). miR-30a was also found to be negatively associated with the expression of N-cadherin, a mesenchymal marker (2), and miR-30d was demonstrated to inhibit tumor growth and invasion in NSCLC (15). However, the possible role of miR-30a in lung cancer remains to be elucidated.…”

Section: Introductionmentioning

confidence: 79%

Absent expression of miR‑30a promotes the growth of lung cancer cells by targeting MEF2D

2018

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Abstract. The microRNA (miR)-30 family has been reported to be aberrantly expressed in several types of cancer. However, its contributions to lung cancer remain to be fully elucidated. Myocyte enhancer factor 2D (MEF2D), an oncogene in liver cancer, has been shown to be aberrantly expressed in lung cancer. In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples. Using an online database, it was predicted that miR-30a targeted the 3' untranslated region (UTR) of MEF2D mRNA. The activity of luciferase with MEF2D 3'UTR was suppressed by transfecting cells with miR-30a mimics. The results of western blot analysis showed that the miR-30a mimics also suppressed the MEF2D protein. The miR-30a mimics were able to reduce the growth and colonies of lung cancer cells by suppressing MEF2D. The results of FACS and western blot assays showed that the apoptotic rate was reduced by transfection with the miR-30a mimics. Collectively, the aberrant expression of miR-30a in lung cancer promoted the expression of MEF2D protein. miR-30a inhibited the growth and colony formation of the lung cancer cells by promoting apoptosis.

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miR‐30d is related to asbestos exposure and inhibits migration and invasion in NCI‐H2452 cells

Yin

et al. 2017

FEBS Open Bio

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Pleural malignant mesothelioma (MM) is a highly aggressive tumor that is typically related to asbestos exposure and has a latency of 20–60 years. Several microRNA contribute to MM initiation and progression, but the mechanisms are not clear. Here, we found that miR‐30d is downregulated in the pleural MM cell line NCI‐H2452, in the plasma of asbestos‐exposed individuals, and in asbestos‐exposed mesothelial cells. Furthermore, we investigated the influence of the overexpression of miR‐30d in pleural MM cells. We demonstrated that miR‐30d overexpression could suppress pleural MM cell proliferation, migration, and invasion in vitro and could promote cell apoptosis but could not significantly influence cell cycle. The mRNA and protein expression of vimentin and TWIST1 decreased, and the mRNA expression of CDH1 increased in NCI‐H2452 cells that overexpressed miR‐30d. We therefore conclude that miR‐30d is related to asbestos exposure and inhibits cell migration and invasion by regulating the epithelial–mesenchymal transition in NCI‐H2452 cells.

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MicroRNA-30d-5p inhibits tumour cell proliferation and motility by directly targeting CCNE2 in non-small cell lung cancer

Cited by 105 publications

References 26 publications

Expression Signature and Role of miR-30d-5p in Non-Small Cell Lung Cancer: a Comprehensive Study Based on in Silico Analysis of Public Databases and in Vitro Experiments

Expression Signature and Role of miR-30d-5p in Non-Small Cell Lung Cancer: a Comprehensive Study Based on in Silico Analysis of Public Databases and in Vitro Experiments

Absent expression of miR‑30a promotes the growth of lung cancer cells by targeting MEF2D

miR‐30d is related to asbestos exposure and inhibits migration and invasion in NCI‐H2452 cells

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