Clinicopathological and prognostic significance of long noncoding RNA MALAT1 in human cancers: a review and meta-analysis

Li, Juan; Cui, Zhigang; Li, Hang; Lv, Xiaoting; Gao, Min; Yang, Zitai; Bi, Yanhong; Zhang, Ziwei; Wang, Shengli; Zhou, Baosen; Yin, Zhihua

doi:10.1186/s12935-018-0606-z

Cited by 29 publications

(21 citation statements)

References 82 publications

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“…MALAT-1 has also been shown to induce epithelial-mesenchymal transition through the miR-204/ZEB2 axis in breast cancer [16]. A previous meta-analysis has shown that the up-regulation of MALAT-1 is significantly correlated with the prognosis and metastasis of cancers [17]. Nevertheless, the prognostic role of MALAT-1 in breast cancer is poorly characterized, with no systematic evaluation conducted to date [18,19].…”

Section: Introductionmentioning

confidence: 99%

Elevated long noncoding RNA MALAT-1 expression is predictive of poor prognosis in patients with breast cancer: a meta-analysis

Wang

Zhang

et al. 2020

Bioscience Reports

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Accumulating evidence indicates that aberrant regulation of metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1), a long noncoding RNA, plays a vital role in tumorigenesis. However, its association with breast cancer has not been systematically evaluated. In the current study, a meta-analysis was conducted to clarify the association between MALAT-1 and the prognosis and clinicopathological features of breast cancer. Relevant literature published in several databases was searched. Hazard ratio (HR) and odds ratio (OR) with 95% confidence interval (CI) were calculated to evaluate the effect of MALAT-1 expression on the survival outcomes and clinicopathological features of breast cancer. A total of 12 studies involving 4,106 patients were identified. Pooled HR demonstrated that elevated MALAT-1 expression significantly predicted unfavorable overall survival (HR=2.06, 95% CI: 1.66–2.56, P<0.0001) in patients with breast cancer. Subgroup analysis stratified by cancer type, sample size, and method of variance analysis also showed statistically significant associations. Additionally, the HR of patients with upregulated MALAT-1 expression concerning disease-free survival, recurrence-free survival, and disease-specific survival was 1.91 (95% CI: 1.53–2.39, P<0.0001). Further, elevated MALAT-1 expression was positively correlated with the progesterone receptor status (OR=1.47, 95% CI: 1.18–1.82). Thus, MALAT-1 is a promising biomarker for predicting survival outcomes in patients with breast cancer.

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Section: Introductionmentioning

confidence: 99%

Elevated long noncoding RNA MALAT-1 expression is predictive of poor prognosis in patients with breast cancer: a meta-analysis

Wang

Zhang

et al. 2020

Bioscience Reports

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“…However, autophagy inhibition caused by increased MALAT1 has been rarely reported and investigated. For autophagy regulation, it is widely accepted that the mammalian target of rapamycin complex 1 (mTORC1) from the autophagy-inhibiting PI3k-Akt pathway [26] and increased MALAT1 could activate PI3K-AKT pathway in numerous cancers including GC [27]. In this study, we demonstrated that increased MALAT1 could inhibit autophagy ux through activating AKT/mTOR pathway.…”

Section: Discussionmentioning

confidence: 67%

MALAT1 Induces Fibroblast Activation to Promote Cancer Progression via Blunting Autophagic Flux and Instigating IL-6 Secretion in Gastric Cancer Cells

Wang¹,

Wang²,

Zhang³

et al. 2020

Preprint

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BackgroundAutophagy defection contributes to inflammation dysregulation, which plays an important role in gastric cancer (GC) progression. Various studies have demonstrated that long noncoding RNA could function as novel regulators of autophagy. However, the epigenetic regulatory mechanisms by which blockage of autophagy caused by long noncoding RNAs develops cancer progression remain unclear. This study aimed to investigate the role of the long noncoding RNA MALAT1 in the autophagy related inflammation dysregulation of GC progression and elucidate the underlying molecular mechanisms.MethodsThe effect of MALAT1 on autophagy in GC cells was analysed by immunoblotting, immunofluorescence and transmission electron microscopy. The role of MALAT1 in regulating inflammation dysregulation was evaluated by ELISA, qPCR and immunoblotting. Bioinformatic prediction, RNA immunoprecipitation-qRCP and immunofluorescence were performed to identify the competitive binding relationship among MALAT1, ELAVL1 and PTEN 3'-UTRs.The chromatin immunoprecipitation assay was performed to examine STAT3 interaction in the MALAT1 promoter region. Immunoblotting was performed to identify the PTEN/AKT/mTOR and SQSTM1/NF-kb mediated pathways altered by MALAT1. The influence of MALAT1 on fibroblasts activation were determined both in in vitro and in vivo.ResultsWe found that the long noncoding RNA MALAT1 could promote interleukin-6 (IL-6) secretion in GC cells by blocking autophagic flux. Moreover, IL-6 induced by MALAT1 could activate normal to cancer-associated fibroblast conversion. The interaction between GC cells and cancer-associated fibroblasts in the tumour microenvironment could facilitate cancer progression. Mechanistically, MALAT1 overexpression destabilized the PTEN mRNA in GC cells by competitively interacting with the RNA-binding protein ELAVL1 to activate the AKT/mTOR pathway for impairing autophagic flux. As the consequence of autophagy inhibition, SQSTM1 accumulation promotes NF-κB translocation to elevate IL-6 expression. Furthermore, STAT3 induced by IL-6 is responsible for upregulation of MALAT1 in GC.ConclusionsOverall, these results demonstrated that intercellular interaction between GC cells and fibroblasts was mediated by autophagy inhibition caused by increased MALAT1 that promote GC progression, providing novel prevention and therapeutic strategies for GC.

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“…MALAT1 overexpression was first described in cancer ( 76 ) and in response to 24 h hypoxic stimulus ( 77 , 78 ). However, there is increasing evidence that the direction of MALAT1 deregulation is dependent on the disease context ( 79 ) and recently MALAT1 was described to be downregulated in tissue samples from atherosclerotic coronary artery plaques ( 80 ). This is in line with our findings, were MALAT1 was downregulated in both primary and restenotic lesions.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Profiling of Hypoxia-Regulated Non-coding RNAs in Human Primary Endothelial Cells

Moreau

Örd

Downes

et al. 2018

Front. Cardiovasc. Med.

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Hypoxia occurs in human atherosclerotic lesions and has multiple adverse effects on endothelial cell metabolism. Recently, key roles of long non-coding RNAs (lncRNAs) in the development of atherosclerosis have begun to emerge. In this study, we investigate the lncRNA profiles of human umbilical vein endothelial cells subjected to hypoxia using global run-on sequencing (GRO-Seq). We demonstrate that hypoxia regulates the nascent transcription of ~1800 lncRNAs. Interestingly, we uncover evidence that promoter-associated lncRNAs are more likely to be induced by hypoxia compared to enhancer-associated lncRNAs, which exhibit an equal distribution of up- and downregulated transcripts. We also demonstrate that hypoxia leads to a significant induction in the activity of super-enhancers next to transcription factors and other genes implicated in angiogenesis, cell survival and adhesion, whereas super-enhancers near several negative regulators of angiogenesis were repressed. Despite the majority of lncRNAs exhibiting low detection in RNA-Seq, a subset of lncRNAs were expressed at comparable levels to mRNAs. Among these, MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia.

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Clinicopathological and prognostic significance of long noncoding RNA MALAT1 in human cancers: a review and meta-analysis

Cited by 29 publications

References 82 publications

Elevated long noncoding RNA MALAT-1 expression is predictive of poor prognosis in patients with breast cancer: a meta-analysis

Elevated long noncoding RNA MALAT-1 expression is predictive of poor prognosis in patients with breast cancer: a meta-analysis

MALAT1 Induces Fibroblast Activation to Promote Cancer Progression via Blunting Autophagic Flux and Instigating IL-6 Secretion in Gastric Cancer Cells

Transcriptional Profiling of Hypoxia-Regulated Non-coding RNAs in Human Primary Endothelial Cells

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