Non-coding RNAs participate in the regulatory network of CLDN4 via ceRNA mediated miRNA evasion

Song, Yongxi; Sun, Jingwei; Zhao, Jiang; Yang, Yuchong; Shi, Jinxin; Wu, Zhonghua; Chen, Xiaowan; Gao, Peng; Zhang, Miao; Wang, Zhenning

doi:10.1038/s41467-017-00304-1

Cited by 234 publications

(217 citation statements)

References 56 publications

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“…It is commonly known that EMT is important for cancer cell invasion and metastasis, including in GC cells . We detected the expression of EMT‐related proteins and found that SIX1 expression negatively correlated with E‐cadherin levels.…”

Section: Discussionmentioning

confidence: 93%

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

Xie

Peng

Sun

et al. 2018

Cell Biochemistry & Function

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Sine oculis homeobox homologue 1 (SIX1) is a Six class homeobox gene conserved throughout many species. It has been reported to act as an oncogene and is overexpressed in many cancers. However, the function and regulatory mechanism of SIX1 in gastric cancer (GC) remains unclear. In our study, we detected protein levels of SIX1 via immunohistochemistry (IHC) and its proliferation and invasion effects via CCK8 and transwell assays. Additionally, expression of cyclin D1, MMP2, p‐ERK, and EMT‐related proteins was measured by western blotting. We found that SIX1 had significantly higher expression in GC tissues and that it could promote GC cell proliferation and invasion. Also, overexpression of SIX1 increased the expression of cyclin D1, MMP2, p‐ERK, and EMT‐related proteins, which could all be inhibited by knocking down SIX1. In conclusion, SIX1 is upregulated in GC tissues. It can promote GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E‐cadherin. Significance of the study Our study showed that SIX1 was upregulated in GC tissues, and promoted GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E‐cadherin. These results suggested the potential regulatory mechanism of SIX1 in proliferation and invasion of gastric cancer.

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Section: Discussionmentioning

confidence: 93%

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

Xie

Peng

Sun

et al. 2018

Cell Biochemistry & Function

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“…The procedure was carried out as previously described . Wt‐MALAT1 and mut‐MALAT1 as well as wt‐HDAC4 and mut‐HDAC4 were transcribed from vector pGEM ® ‐T (Promega) and biotin‐labeled with the Biotin RNA Labeling Mix (Roche, Basel, Switzerland) and T7 RNA polymerase (Roche), treated with RNase‐free DNase I (Roche), and purified with an RNeasy Mini Kit (Qiagen, Valencia, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Long noncoding RNA MALAT1 regulates HDAC4‐mediated proliferation and apoptosis via decoying of miR‐140‐5p in osteosarcoma cells

Sun

Qin

2018

Cancer Medicine

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Noncoding RNAs regulate the initiation and progression of osteosarcoma (OS). The role of long noncoding RNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) playing in OS and whether the function it working out was achieved through HDAC4 pathway remain uncovered. In this study, we illustrated that MALAT1 was upregulated and was correlated with poor prognosis in OS patients. Meanwhile, we demonstrated that a depression of MALAT1 suppressed proliferation and promoted apoptosis in OS cell line HOS and 143B. Further, we verified that MALAT1 exerting its function via upregulating of histone deacetylase 4 (HDAC4). Through an online prediction, a series of luciferase assays and RNA pull‐down assays, we demonstrated that both MALAT1 and HDAC4 were the targets of microRNA‐140‐5p (miR‐140‐5p) via sharing a similar microRNA responding elements. Even further, we revealed that MALAT1 served as a ceRNA of HDAC4 via decoying of miR‐140‐5p. Finally, we proved that MALAT1 promoted OS tumor growth in an in vivo animal study. In summary, the outcomes of this study demonstrated the complex ceRNA network among MALAT, miR‐140‐5p, and HDAC4‐mediated proliferation and apoptosis in OS. This study might provide a new axial in molecular treatment of OS.

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“…The up‐regulation of miR‐29 could reduce lesion size and necrotic zones via targeting Col1A and Col3A . Recently, a novel regulatory mechanism among lncRNAs, miRNAs and their mRNA targets has been annotated in CVDs by pull‐down assay, chromatin immunoprecipitation (ChIP), luciferase reporter gene assay and quantitative reverse transcription polymerase chain reaction (qRT‐PCR) methods, although a plurality of evidence has revealed that lncRNA‐miRNA‐mRNA cascades participated in various pathophysiological processes in the field of oncology . In this review, four kinds of regulatory relationships were summarized: (a) the role of lncRNAs as miRNA sponges; (b) the coexpression of lncRNAs with miRNAs; (c) the reciprocal repression of lncRNAs and miRNAs; and (d) the role of miRNAs as negative regulators of lncRNAs.…”

Section: Introductionmentioning

confidence: 99%

The novel regulatory role of lncRNA‐miRNA‐mRNA axis in cardiovascular diseases

Huang

2018

J Cellular Molecular Medi

368

288

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Long noncoding RNAs (lncRNAs) are RNAs longer than 200 nt in length that are characterized by low levels of sequence conservation and expression; lncRNAs modulate various biological functions at epigenetic, transcriptional and post‐transcriptional levels, or directly regulate protein activity. As a family of small and evolutionarily conserved noncoding RNAs, microRNAs (miRNAs) are capable of regulating physiological and pathological processes via inhibiting target mRNA translation or promoting mRNA degradation. A number of studies have confirmed that both lncRNAs and miRNAs are closely associated with the development of cardiovascular diseases (CVDs), such as cardiac remodelling, heart failure, myocardial injury and arrhythmia, and that they act as biomarkers, potential therapeutic targets or strong indicators of prognosis; however, the underlying molecular mechanism has not been elucidated. Recently, emerging evidence showed that the novel regulatory mechanism underlying the crosstalk among lncRNAs, miRNAs and mRNAs plays a pivotal role in the pathophysiological processes of CVDs in response to stress stimuli. In this review, I comprehensively summarized the regulatory relationship of lncRNAs, miRNAs and mRNAs and highlighted the important role of the lncRNA‐miRNA‐mRNA axis in CVDs.

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Non-coding RNAs participate in the regulatory network of CLDN4 via ceRNA mediated miRNA evasion

Cited by 234 publications

References 56 publications

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

Long noncoding RNA MALAT1 regulates HDAC4‐mediated proliferation and apoptosis via decoying of miR‐140‐5p in osteosarcoma cells

The novel regulatory role of lncRNA‐miRNA‐mRNA axis in cardiovascular diseases

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