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MicroRNA-330-3p functions as an oncogene in human esophageal cancer by targeting programmed cell death 4.

ABSTRACT: MicroRNAs comprise a family of small non-coding RNA molecules that have emerged as key post-transcriptional regulators of gene expression. Aberrant miRNA expression has been linked to various human tumors. This study was aimed to identify novel miRNAs involved in the carcinogenesis of esophageal squamous cell carcinoma (ESCC) and their potential functions. We performed miRNA microarray and found that miR-330-3p was highly expressed in ESCC tumor tissues. qRT-PCR further confirmed the result in other 35 pairs of ESCC tumor tissues and ESCC cell lines. Ectopic expression of miR-330-3p significantly promoted ESCC cell proliferation, survival, migration, invasion in vitro and stimulated tumor formation in nude mice. Knockdown of miR-330-3p leaded to the opposite effects. The luciferase assay confirmed that miR-330-3p directly interacted with the PDCD4 mRNA 3' un-translated region (UTR). Moreover, expression of PDCD4 was inversely associated with miR-330-3p in ESCC tissues. Silencing of PDCD4 significantly promoted cell growth, cell migration, invasion and inhibited cisplatin-induced apoptosis in ESCC cells. This study suggested that miR-330-3p might play an oncogenic role in the development of ESCC partially via suppression of PDCD4 expression.

SUBMITTER: Meng H

PROVIDER: S-EPMC4449435 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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MicroRNA-330-3p functions as an oncogene in human esophageal cancer by targeting programmed cell death 4.

Meng Hui H Wang Kai K Chen Xuedan X Guan Xingying X Hu Liwen L Xiong Gang G Li Juan J Bai Yun Y

American journal of cancer research 20150215 3

MicroRNAs comprise a family of small non-coding RNA molecules that have emerged as key post-transcriptional regulators of gene expression. Aberrant miRNA expression has been linked to various human tumors. This study was aimed to identify novel miRNAs involved in the carcinogenesis of esophageal squamous cell carcinoma (ESCC) and their potential functions. We performed miRNA microarray and found that miR-330-3p was highly expressed in ESCC tumor tissues. qRT-PCR further confirmed the result in o ...[more]

PMID: 26045986

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Project description:One key risk factor of aortic valve stenosis in clinical practice is bicuspid aortic valve (BAV). Increasing evidence indicates that numerous microRNAs (miRs/miRNAs) are involved in BAV calcification via their target genes. miR‑330‑3p was found to be involved in the deterioration of BAV calcification by miR profiling in human calcified BAV and tricuspid aortic valve (TAV) tissues in the present study and the underlying mechanism was investigated. RNA sequencing was performed on four BAV and four TAV tissues from patients with aortic stenosis before these leaflets were examined for the expression levels of miR‑330‑3p and CREB‑binding protein (CREBBP) by reverse transcription‑PCR. The alteration of functional factors associated with calcification was also assessed by Western blotting and immunohistochemistry in human aortic tissue samples. The putative target of miR‑330‑3p was detected by dual‑luciferase assay in 293 cells. Furthermore, the influence of miR‑330‑3p expression on osteogenic progression was explored in cultured porcine valve interstitial cells (VICs). Rescue experiments of CRBBP were performed to confirm the influence of the miR‑330‑3p‑CREBBP pathway in the calcification progress in porcine VICs. RNA sequencing indicated distinct expression of miR‑330‑3p in human BAV tissues compared with TAV, which was then confirmed by PCR. CREBBP expression levels in human BAV and TAV leaflets also demonstrated the opposite alterations. This negative correlation was then confirmed in cultured porcine VICs. Under an osteogenic environment, cellular calcification was promoted in miR‑330‑3p‑overexpressed porcine VICs expressing higher bone morphogenetic protein 2, Runt‑related transcription factor 2, matrix metalloproteinase (MMP)‑2, MMP‑9 and collagen I compared with controls. Rescue experiments further confirmed that miR‑330‑3p played its role via targeting CREBBP in porcine VICs. Collectively, miR‑330‑3p was upregulated in calcified BAV compared with TAV. The upregulation of miR‑330‑3p promotes the calcification progress partially via targeting CREBBP.

Project description:ObjectiveThe aim of this study was to investigate the microRNA-200b-3p expression in lung adenocarcinoma and the possible functional associations of microRNA-200b-3p with cell proliferation, migration, and invasion.MethodsQuantitative real-time polymerase chain reaction was used to detect the expression of microRNA-200b-3p in lung adenocarcinoma samples and in the human lung adenocarcinoma cell lines A549 and H1299. A549 and H1299 cells were transfected with either a microRNA-200b-3p mimic or a negative control microRNA or either an empty vector or an adenosine triphosphate-binding cassette transporter A-1 overexpression vector. A Cell Counting Kit-8 assay was employed to assess the ability of cell proliferation. Transwell assays and transwell-Matrigel invasion assay were, respectively, utilized to assess the capacity of migration and invasion in A549 and H1299 cells.ResultsThe results showed that microRNA-200b-3p expression was significantly upregulated in tumor tissues compared with that in adjacent normal tissues. Overexpression of microRNA-200b-3p promoted lung adenocarcinoma cell proliferation and metastasis. Furthermore, adenosine triphosphate-binding cassette transporter A-1 was a direct target of microRNA-200b-3p, and this binding was verified by luciferase reporter analysis. Overexpression of adenosine triphosphate-binding cassette transporter A-1 obviously suppressed lung adenocarcinoma cell proliferation, migration, and invasion. Lung adenocarcinoma cell phenotypes induced by microRNA-200b-3p overexpression could be partially remitted by the co-overexpression of microRNA-200b-3p and adenosine triphosphate-binding cassette transporter A-1.ConclusionThis study first identified that microRNA-200b-3p is upregulated in lung adenocarcinoma cells and associated with cell proliferation and metastasis. MicroRNA-200b-3p promoted lung adenocarcinoma cell proliferation and metastasis by suppressing adenosine triphosphate-binding cassette transporter A-1. MicroRNA-200b-3p may function as a novel molecular marker and therapeutic target for lung adenocarcinoma treatment.

Project description:BACKGROUND:Discoidin domain receptor-1 (DDR1) tyrosine kinase is highly expressed in a variety of human cancers and involved in various steps of tumorigenesis. However, the precise mechanisms underlying the abnormal expression of DDR1 in oral squamous cell carcinoma (OSCC) has not been well investigated. METHODS:The expression of DDR1 on OSCC patients was determine by quantitative real-time PCR (qRT-PCR) and immunohistochemistry. Specific targeting by miRNAs was determined by software prediction, luciferase reporter assay, and correlation with target protein expression. The functions of miR-486-3p and DDR1 were accessed by MTT and Annexin V analyses using gain- and loss-of-function approaches. Chromatin immunoprecipitation (ChIP) and methylation specific PCR (MSP) were performed to explore the molecular mechanisms by arecoline treatment. RESULTS:Here, we reported that DDR1 was significantly upregulated in OSCC tissues and its levels were inversely correlated with miR-486-3p expression. The experimental results in vitro confirmed that miR-486-3p decreased DDR1 expression by targeting the 3'-UTR of DDR1 mRNA. Overexpression of miR-486-3p led to growth inhibition and apoptosis induction with a similar function by knockdown of DDR1. Aberrant methylation of ANK1 promoter was a highly prevalent in OSCC and contributes to oral carcinogenesis by epigenetic silencing of ANK1 and miR-486-3p. We found that miR-486-3p can be transcriptionally co-regulated with its host gene ANK1 through epigenetic repression. DNA methylation inhibitor treatment re-expressed ANK1 and miR-486-3p. Importantly, arecoline, a major betel nut alkaloid, recruited DNMT3B binding to ANK1 promoter for DNA methylation and then attenuated the expression of miR-486-3p in OSCC. CONCLUSION:This study was the first to demonstrate that betel nut alkaloid may recruit DNMT3B to regulate miR-486-3p/DDR1 axis in oral cancer andmiR-486-3p and DDR1 may serve as potential therapeutic targets of oral cancer.

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MicroRNA-330-3p functions as an oncogene in human esophageal cancer by targeting programmed cell death 4.

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MicroRNA-330-3p functions as an oncogene in human esophageal cancer by targeting programmed cell death 4.

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