Silencing of Long Noncoding RNA MALAT1 by miR-101 and miR-217 Inhibits Proliferation, Migration, and Invasion of Esophageal Squamous Cell Carcinoma Cells

Wang, Xinyu; Li, Meng; Wang, Zhiqiong; Han, Sichong; Tang, Xiaohu; Ge, Yunxia; Zhou, Lixin; Zhou, Changchun; Yuan, Qipeng; Yang, Ming

doi:10.1074/jbc.m114.596866

Cited by 266 publications

(229 citation statements)

References 44 publications

(39 reference statements)

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“…Our results indicated that the direct binding ability of the miR-101b on the MALALT1 transcript, in line with the previous report. 27 Additionally, we identified Rac1 as a new target of miR-101b in liver fibrosis, which amplifies the repertoire of miR-101b targets. Several studies have reported that Rac1 signaling is involved in the pathogenesis of liver fibrosis.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that miR-101b is downregulated in liver fibrosis, 7 which was confirmed by our data. Wang et al 27 demonstrated that miR-101 can inhibit MALAT1 expression in esophageal squamous cell carcinoma. However, whether MALAT1 can regulate miR-101 expression has not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…27 Here we examined the expression of MALAT1 and miR-101b in normal and fibrotic liver tissues. Our results indicated that the expression of miR-101b was down-regulated by 48% in the CCl 4 group compared with the control group (Fig.…”

Section: Knockdown Of Malat1 Alleviates Mouse Liver Fibrosis In Vivomentioning

confidence: 99%

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MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis

Cai

et al. 2015

Cell Cycle

112

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Abbreviations: a-SMA, smooth muscle a-actin; Ad-shCtrl, adenoviral vectors expressing the scrambled shRNA; Ad-shMALAT1, adenoviral vectors expressing shRNA against MALAT1. EdU, 5-Ethyny-2 0 -deoxyuridine; Ago2, Argonaute-2; BDL, bile duct ligation; CCl 4 , carbon tetrachloride; ceRNAs, competing endogenous RNAs; Col1a1, collagen type I, a 1; DMEM, Dulbecco's modified Eagle's medium; HSCs, hepatic stellate cells; IgG, immunoglobulin G; IHC, immunohistochemical; lncRNAs, long noncoding RNAs; MALAT1, Metastasis-associated lung adenocarcinoma transcript 1; miR-101, microRNA-101; miR-NC, miR-101b negative control; miRNAs, microRNAs; ncRNAs, non-coding RNAs; qRT-PCR, quantitative real-time PCR; Rac1, RAS-related C3 botulinum substrate 1; siCtrl, scrambled siRNA; siRNAs, small interfering RNAs.Emerging evidence shows that Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a pivotal role in cell proliferation, migration, and invasion in tumors. However, the biological role and underlying mechanism of MALAT1 in liver fibrosis remains undefined. In this study, up-regulation of MALAT1 was observed in fibrotic liver tissues and in activated hepatic stellate cells (HSCs). In addition, depletion of MALAT1 inhibited the activation of HSCs in vitro and attenuated collagen deposits in vivo. Our results demonstrated that MALAT1 expression is negatively correlated with microRNA-101b (miR-101b) expression. Furthermore, there was a negative feedback loop between the levels of MALAT1 and miR-101b. Luciferase reporter assay indicated that MALAT1 and RAS-related C3 botulinum substrate 1 (Rac1) are targets of miR-101b. We uncovered that MALAT1 regulates Rac1 expression through miR-101b as a competing endogenous RNA (ceRNA), thereby influencing the proliferation, cell cycle and activation of primary HSCs. Collectively, The ceRNA regulatory network may prompt a better understanding of liver fibrogenesis and contribute to a novel therapeutic strategy for liver fibrosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis

Cai

et al. 2015

Cell Cycle

112

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“…The elevation of MALAT1 is achieved through the following: (1) transcriptional activation on the epigenetic level such as demethylation of histone H3K9 28 or on the genetic level such as through transforming growth factor-β (TGF-β), 29 cyclic AMPresponsive element binding (CREB), 30 Wnt/β-catenin pathway, 31 or SOX17; 32 (2) post-transcriptional regulation, such as miRNA-mediated silencing, as demonstrated by miR-125, 33 miR-9, 34 miR-101, and miR-217. 35 In addition to functioning as a marker for malignancy, MALAT1 upregulation significantly correlates with the poor prognosis of cancer patients, rendering this molecule a prognostic indicator. [36][37][38] In this study, we found that MALAT1 and miR-204 mutually and negatively regulated the expression of each other, and their levels negatively correlated with each other in HCC tissues, suggesting that although miR-204 could control the expression of MALAT1, the upregulation of MALAT1 in HCC tissues would downregulate the level of miR-204, which in turn further elevates MALAT1 and exacerbates the phenotypes induced by MALAT1.…”

Section: Discussionmentioning

confidence: 99%

The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1

Hou

Zhou

et al. 2017

Tumour Biol.

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Increasing evidence supports the significance of long non-coding RNA in cancer development. Several recent studies suggest the oncogenic activity of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in hepatocellular carcinoma. In this study, we explored the molecular mechanisms by which MALAT1 modulates hepatocellular carcinoma biological behaviors. We found that microRNA-204 was significantly downregulated in sh-MALAT1 HepG2 cell and 15 hepatocellular carcinoma tissues by quantitative real-time polymerase chain reaction analysis. Through bioinformatic screening, luciferase reporter assay, RNA-binding protein immunoprecipitation, and RNA pull-down assay, we identified microRNA-204 as a potential interacting partner for MALAT1. Functionally, wound-healing and transwell assays revealed that microRNA-204 significantly inhibited the migration and invasion of hepatocellular carcinoma cells. Notably, sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process. These data elucidated, by sponging and competitive binding to microRNA-204, MALAT1 releases the suppression on sirtuin 1, which in turn promotes hepatocellular carcinoma migration and invasion. This study reveals a novel mechanism by which MALAT1 stimulates hepatocellular carcinoma progression and justifies targeting metastasis-associated lung adenocarcinoma transcript 1 as a potential therapy for hepatocellular carcinoma.

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“…In oesophageal squamous cell carcinoma, silencing the MALAT1 expression resulted in the inhabitation of proliferation, migration, and invasion [57,58]. Other studies also reported the deregulation of MALAT1 in bladder cancer and renal cancers [59,60].…”

Section: Metastasis-associated Lung Adenocarcinoma Transcript 1 (Malat1)mentioning

confidence: 91%

Long Non-Coding RNA in Non-Small Cell Lung Cancers

Cheng¹,

Mao²

2017

A Global Scientific Vision - Prevention, Diagnosis, and Treatment of Lung Cancer

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Non-small cell lung cancer (NSCLC) accounts for nearly 80% of diagnosed lung cancers. Due to the predominantly late diagnosis of NSCLC and drug resistance in the targeted therapy approaches, the 5-year overall survival rate is still less than 19%. Thus, novel diagnosis and treatment approaches are needed. Many eforts have been made to achieve great progress in understanding the genomic landscape of NSCLC and the molecular mechanisms involved in tumorigenesis. Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides with litle or no protein-coding potential.They are encoded across the genome and are involved in a wide range of cellular and biological processes. Dysregulation of lncRNAs is associated with a number of cancerrelated processes, including epigenetic regulation, microRNA silencing, and DNA damage. Furthermore, lncRNAs have been reported to have the potential as biomarker for diagnosis and prognosis, as well as the therapy targets. Here in this chapter, we review some well-characterized lncRNAs associated with NSCLCs and the potential of lncRNAs as biomarkers in the diagnosis and prognosis of NSCLCs.

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Silencing of Long Noncoding RNA MALAT1 by miR-101 and miR-217 Inhibits Proliferation, Migration, and Invasion of Esophageal Squamous Cell Carcinoma Cells

Cited by 266 publications

References 44 publications

MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis

MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis

The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1

Long Non-Coding RNA in Non-Small Cell Lung Cancers

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