LncBRM initiates YAP1 signalling activation to drive self-renewal of liver cancer stem cells

Zhu, Pingping; Wang, Yanying; Wu, Jiayi; Huang, Guanling; Liu, Benyu; Ye, Buqing; Du, Ying; Gao, Guangxia; Tian, Yong; He, Lei; Fan, Zusen

doi:10.1038/ncomms13608

Cited by 243 publications

(197 citation statements)

References 54 publications

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“…Multiple lncRNAs have been implicated to be crucial modulators in regulating cell behaviors and eventually modulating tumor progression, however, most of them are still not functionally defined. For instance, LncBRM was reported to maintain the renewal of liver cancer stem cell via imitating the YAP1 signaling pathway . In addition, lncRNA TP73‐AS1 overexpression was found has connection with survival quality of glioblastoma, and promotes tumorigenesis and temozolomide resistant .…”

Section: Discussionmentioning

confidence: 99%

LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

Kang

Shi

et al. 2019

BioFactors

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Non‐small cell lung cancer (NSCLC) accounts for about 80% of lung cancers worldwide. In recent years, importance of noncoding RNAs including long noncoding RNA and microRNA in regulating tumor progression has been appreciated. Abnormally expression of DiGeorge syndrome critical region gene 5 (DGCR5) was found in multiple human cancers but its function in NSCLC is largely unknown. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) was conducted to explore DGCR5 expression level in NSCLC. Bioinformatic analyses were conducted to explore the targets of DGCR5. Cell counting kit‐8 assay, wound‐healing assay, and transwell invasion assay were performed to analyze functions of DGCR5. RT‐qPCR revealed that DGCR5 expression in NSCLC cells was significantly lower than in normal cell. DGCR5 overexpression suppresses NSCLC cell growth, migration, and invasion. Online algorithms found EPH receptor B6 (EPHB6) and DGCR5 contains same miR‐211‐5p binding region. The predicted connections were further validated by luciferase activity reporter assay. Recue experiments showed DGCR5 regulates NSCLC cell behaviors via targeting miR‐211‐5p/EPHB6. These findings collectively identified DGCR5/miR‐211‐5p/EPHB6 triple axis in NSCLC, which may novel understanding regarding the tumorigenesis of NSCLC.

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Section: Discussionmentioning

confidence: 99%

LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

Kang

Shi

et al. 2019

BioFactors

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“…Long noncoding RNAs (lncRNAs) are evolutionarily conserved RNAs with no functional protein‐coding ability (Guttman, Russell, Ingolia, Weissman, & Lander, ). Increasing evidence has shown that lncRNAs are responsible for essential gene regulatory functions in various tissues (Guttman et al, ; Liu et al, ; Zhu et al, ). As in brain, research has shown that many lncRNAs are highly expressed in the brain (Kiang, Zhang, & Leung, ), and taken specific expression means specific function into consideration, high expression means important functions in normal brain development and brain‐related diseases, such as glioma (Y. Wang & Lan, ; O. Wang et al, ; Yu et al, ).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA gastric cancer‐associated transcript 3 plays oncogenic roles in glioma through sponging miR‐3127‐5p

Pan

Zhao

2018

Journal Cellular Physiology

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Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer‐associated transcript 3 (GACAT3) is reported to participate in the development of breast cancer, colorectal cancer, nonsmall cell lung cancer, and gastric cancer. However, whether it is implicated in glioma has not been elucidated. Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines. Higher GACAT3 expression predicted lower survival rate. Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells. Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)‐3127‐5p. Subsequently, ELAVL1 was identified as a direct target of miR‐3127‐5p by bioinformatics analysis and luciferase reporter assay. Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR‐3127‐5p, leading to glioma progression. Taken together, our study elucidated that GACAT3/miR‐3127‐5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target.

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“…Discussion lncRNAs are involved in regulating gene expression and widen our understanding of its biological functions in diseases, including cancers [33,34]. Emerging evidence has demonstrated the functions of lncRNAs in HCC, including lncRNA-PVT1 [7][8][9][10]35]. As reported by xu et al, the overexpression of PVT1 in gastric cancer can predict the poor prognosis of gastric cancer patients and promote tumor cell proliferation and invasion via binding to FOXM1 [15].…”

Section: The Potential Pathways Associated With Pvt1 and Mir-424-5pmentioning

confidence: 88%

“…It has been indicated has lncRNAs could affect different cellular functions and participate in various physiological and pathological progress [6]. Accumulating evidence has shown that the ectopic expression of lncRNAs could influence the progression of HCC by modulating the self-renewal ability of liver cancer stem cells (CSCs) and other biological functions, including proliferation, apoptosis, invasion, and metastasis [7][8][9][10]. Moreover, other articles have also reported that the aberrant expression of lncRNAs might be involved in regulating the chemotherapy resistance of HCC patients [11,12].…”

Section: Introductionmentioning

confidence: 99%

A Preliminary Investigation of PVT1 on the Effect and Mechanisms of Hepatocellular Carcinoma: Evidence from Clinical Data, a Meta-Analysis of 840 Cases, and In Vivo Validation

Wen

Zhang

Huang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hepatocellular carcinoma (HCC) remains a difficult problem that significantly affects the survival of the afflicted patients. Accumulating evidence has demonstrated the functions of long non-coding RNA (lncRNA) in HCC. In the present study, we aimed to explore the potential roles of PVT1 in the tumorigenesis and progression of HCC. Methods: In this study, quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was applied to detect the differences between PVT1 expression in HCC tissues and cell lines. Then, the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were searched to confirm the relationship between PVT1 expression and HCC. Moreover, a meta-analysis comprising TCGA, GEO, and RT-qPCR was applied to estimate the expression of PVT1 in HCC. Then, cell proliferation was evaluated in vitro. A chicken chorioallantoic membrane (CAM) model of HCC was constructed to measure the effect on tumorigenicity in vivo. To further explore the sponge microRNA (miRNA) of PVT1 in HCC, we used TCGA, GEO, a gene microarray, and target prediction algorithms. TCGA and GEO and the gene microarray were used to select the differentially expressed miRNAs, and the different target prediction algorithms were applied to predict the target miRNAs of PVT1. Results: We found that PVT1 was markedly overexpressed in HCC tissue than in normal liver tissues based on both RT-qPCR and data from TCGA, and the overexpression of PVT1 was closely related to the gender and race of the patient as well as to higher HCC tumor grades. Also, a meta-analysis of 840 cases from multiple sources (TCGA, GEO and the results of our in-house RT-qPCR) showed that PVT1 gained moderate value in discriminating HCC patients from normal controls, confirming the results of RT-qPCR. Additionally, the upregulation of PVT1 could promote HCC cell proliferation in vitro and vivo. Based on the competing endogenous RNA (ceRNA) theory, the PVT1/miR-424-5p/INCENP axis was finally selected for further research. The in silico prediction revealed that there were complementary sequences between PVT1 and miR-424-5p as well as between miR-424-5p and INCENP. Furthermore, a negative correlation trend was found between miR-424-5p and PVT1 based on RT-qPCR, whereas a positive correlation trend was found between PVT1 and INCENP based on data from TCGA. Also, INCENP small interfering RNA (siRNA) could significantly inhibit cell proliferation and viability. Conclusions: We hypothesized that PVT1 could affect the biological function of HCC cells via targeting miR-424-5p and regulating INCENP. Focusing on the new insight of the PVT1/miR-424-5p/INCENP axis, this study provides a novel perspective for HCC therapeutic strategies.

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LncBRM initiates YAP1 signalling activation to drive self-renewal of liver cancer stem cells

Cited by 243 publications

References 54 publications

LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

Long noncoding RNA gastric cancer‐associated transcript 3 plays oncogenic roles in glioma through sponging miR‐3127‐5p

A Preliminary Investigation of PVT1 on the Effect and Mechanisms of Hepatocellular Carcinoma: Evidence from Clinical Data, a Meta-Analysis of 840 Cases, and In Vivo Validation

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