Loss‐of‐function of miR‐142 by hypermethylation promotes <scp>TGF</scp>‐β‐mediated tumour growth and metastasis in hepatocellular carcinoma

Yu, Qian; Xiang, Leyang; Yin, Libo; Liu, Xincheng; Yang, Dian; Zhou, Jianyin

doi:10.1111/cpr.12384

Cited by 43 publications

(29 citation statements)

References 26 publications

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“…MiR-142-3p is a well-established tumor suppressive miRNA and has regulatory roles in multiple cell behaviors, such as migration and invasion. A recent study reported that miR-142 is hypermethylated in liver cancer [17]. Our study also observed the methylation of miR-142 in NSCLC cells.…”

Section: Discussionsupporting

confidence: 85%

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LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1

Wei

Liu

et al. 2020

BMC Pulm Med

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Background: This study aimed to investigate the role of MIR17HG in non-small cell lung cancer (NSCLC). Methods: Differential expression of MIR17HG in NSCLC was first detected by exploring the TCGA dataset. Expression levels of miR-142-3p in both NSCLC and non-tumor tissues were determined by qPCR. The effects of overexpressing MIR17HG on the methylation of miR-142 were assessed by MSP. The effects of overexpressing MIR17HG, miR-142-3p and Bach-1 on the invasion and migration of NSCLC cells were assessed by Trasnwell invasion or migration assay. Results: Analysis of TCGA dataset revealed slightly downregulated expression of MIR17HG in NSCLC. This downregulation was further confirmed by measuring the expression levels of MIR17HG in NSCLC and non-tumor tissues from NSCLC patients. MIR17HG was found to decrease the methylation of miR-142-3p, and overexpression of MIR17HG led to upregulated miR-142-3p. Moreover, overexpression of MIR17HG also led to downregulated Bach-1, the downstream target of miR-142-3p. Cell invasion and migration analysis showed that overexpression of MIR17HG and miR-142-3p led to inhibited cancer cell invasion and migration. In contrast, overexpression of Bach-1 played an opposite role and attenuated the effects of overexpressing MIR17HG and miR-142-3p. Conclusion: MIR17HG inhibits NSCLC by upregulating miR-142-3p to downregulate Bach-1.

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Section: Discussionsupporting

confidence: 85%

“…It is commonly observed that tumor suppressive miRNAs are frequently methylated in cancers [15][16][17]. For instance, miR-145 is regulated by DNA methylation in prostate cancer [15].…”

Section: Discussionmentioning

confidence: 99%

LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1

Wei

Liu

et al. 2020

BMC Pulm Med

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“…The negative controls (NC) were scrambled oligonucleotides. Cell transfection was performed as described previously . Briefly, the miR‐552 mimics, inhibitors and NC purchased from RiboBio (Guangzhou, China) were transfected into cells at a concentration of 100 nmol/L via Lipofectamine 3000 (Invitrogen) according to the manufacturer's protocol.…”

Section: Methodsmentioning

confidence: 99%

MiR‐552 promotes the proliferation, migration and EMT of hepatocellular carcinoma cells by inhibiting AJAP1 expression

Wen

et al. 2018

J Cellular Molecular Medi

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Our goal was to explore the function of miR‐552 and its potential target AJAP1 in hepatocellular carcinoma (HCC) oncogenesis and progression. In this study, bioinformatics analysis was performed to detect abnormally expressed miRNAs. The relationship between miR‐552 and AJAP1 was validated using luciferase reporter assays. RT‐qPCR and Western blot assays were applied to explore the expression level of miR‐552, AJAP1 and epithelial‐mesenchymal transition (EMT) markers. HCC cell proliferation was examined using CCK8 assays, while migration and invasion were investigated using Transwell assays. Nude mouse tumourigenesis models were established to facilitate observation of HCC progression in vivo. Finally, prognostic analysis was performed to discover how the prognosis of HCC patients correlated with miR‐552 and AJAP1 expression. MiR‐552 overexpression in HCC cells promoted HCC cell migration, invasion and EMT by targeting/suppressing AJAP1. Poorer prognosis appeared in HCC patients with higher miR‐552 expression or lower AJAP1 levels. Our findings suggested that miR‐552 promotes HCC oncogenesis and progression by inhibiting AJAP1 expression.

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“…Several studies reported that hypermethylation and/or demethylation of miRNA promoters can influence expression of EMT progression, such as for miR-211 [ 258 , 259 ] in melanoma cells, miR-129 [ 260 ] in HCC, miR-124 [ 261 ] in endometrial cancer, and miR-200 [ 262 ] and miR-203 [ 263 ] in distinct cell types. In some cases, epigenetic modulation of miRNA expression leads to up-regulation of TGF-β signaling such as for miR-142 [ 264 ] in HCC or to epigenetic modulators such as HDAC5 [ 265 ] in NSCLC. Alternatively, miRNAs can directly target epigenetic modulators such as DNMT1 by miR-152 [ 266 ] or lysine K demethylase 6B by miR-941 [ 267 ] leading to impaired EMT development, respectively.…”

Section: Contribution Of Micrornas To Epithelial-to-mesenchymal Trmentioning

confidence: 99%

Functional Role of Non-Coding RNAs during Epithelial-To-Mesenchymal Transition

Expósito-Villén

Aránega

Franco

2018

ncRNA

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Epithelial-to-mesenchymal transition (EMT) is a key biological process involved in a multitude of developmental and pathological events. It is characterized by the progressive loss of cell-to-cell contacts and actin cytoskeletal rearrangements, leading to filopodia formation and the progressive up-regulation of a mesenchymal gene expression pattern enabling cell migration. Epithelial-to-mesenchymal transition is already observed in early embryonic stages such as gastrulation, when the epiblast undergoes an EMT process and therefore leads to the formation of the third embryonic layer, the mesoderm. Epithelial-to-mesenchymal transition is pivotal in multiple embryonic processes, such as for example during cardiovascular system development, as valve primordia are formed and the cardiac jelly is progressively invaded by endocardium-derived mesenchyme or as the external cardiac cell layer is established, i.e., the epicardium and cells detached migrate into the embryonic myocardial to form the cardiac fibrous skeleton and the coronary vasculature. Strikingly, the most important biological event in which EMT is pivotal is cancer development and metastasis. Over the last years, understanding of the transcriptional regulatory networks involved in EMT has greatly advanced. Several transcriptional factors such as Snail, Slug, Twist, Zeb1 and Zeb2 have been reported to play fundamental roles in EMT, leading in most cases to transcriptional repression of cell–cell interacting proteins such as ZO-1 and cadherins and activation of cytoskeletal markers such as vimentin. In recent years, a fundamental role for non-coding RNAs, particularly microRNAs and more recently long non-coding RNAs, has been identified in normal tissue development and homeostasis as well as in several oncogenic processes. In this study, we will provide a state-of-the-art review of the functional roles of non-coding RNAs, particularly microRNAs, in epithelial-to-mesenchymal transition in both developmental and pathological EMT.

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Loss‐of‐function of miR‐142 by hypermethylation promotes TGF‐β‐mediated tumour growth and metastasis in hepatocellular carcinoma

Abstract: These findings implicated that miR-142 was a tumour suppressor gene in HCC and often hyermethylated to increase TGF-β-induced development of hepatocellular carcinoma.

Cited by 43 publications

References 26 publications

LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1

LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1

MiR‐552 promotes the proliferation, migration and EMT of hepatocellular carcinoma cells by inhibiting AJAP1 expression

Functional Role of Non-Coding RNAs during Epithelial-To-Mesenchymal Transition

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