miR‐381‐3p restrains cervical cancer progression by downregulating FGF7

Shang, Anquan; Zhou, Cheng; Bian, Ganxia; Chen, Wei; Lu, Wenying; Wang, Weiwei; Li, Dong

doi:10.1002/jcb.27438

Cited by 53 publications

(41 citation statements)

References 24 publications

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“…14 Recent studies have suggested that miR-381-3p level was decreased in several cancers and overexpression of miR-381-3p inhibited cell proliferation and metastasis, and induced cell cycle arrest and apoptosis. [15][16][17][18][19] However, the functions and mechanisms of miR-381-3p in NPC are still unclear. In our study, miR-381-3p was observed to be down-regulated in NPC.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA DLEU1 Up-Regulates BIRC6 Expression by Competitively Sponging miR-381-3p to Promote Cisplatin Resistance in Nasopharyngeal Carcinoma

Li¹,

Huang²,

Yu³

et al. 2020

OTT

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Background: Cisplatin (DDP) resistance has become an obstacle to chemotherapy for nasopharyngeal carcinoma (NPC) patients. Recent evidences indicate that long noncoding RNAs (lncRNAs) are involved in tumorigenesis and chemoresistance. However, the potential role of lncRNAs in NPC progression remains largely unknown. Methods: First, lncRNA expression profiling in NPC was performed via microarray analysis. To explore the involvement of DLEU1 in DDP resistance, loss-of-function experiments were employed in vitro and in vivo. Bioinformatics analysis, luciferase reporter assay, qRT-PCR, and Western blot assays were used to investigate the underlying mechanisms. Results: Here, we identified 153 differentially expressed lncRNAs. Among them, DLEU1 was remarkably up-regulated in NPC tissues and associated with worse outcome. Knockdown of DLEU1 could sensitize NPC cells to DDP in vitro and in vivo. Further investigations revealed that DLEU1 positively regulated BIRC6 expression via its competing endogenous RNA (ceRNA) activity on miR-381-3p. We also observed that BIRC6 overexpression or miR-381-3p silence could significantly reverse DLEU1-dependent DDP resistance. Conclusion: Our data suggest that DLEU1 acts as an oncogene to promote DDP resistance and BIRC6 expression in NPC through interacting with miR-381-3p, which may help to develop new strategy against NPC chemoresistance.

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Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA DLEU1 Up-Regulates BIRC6 Expression by Competitively Sponging miR-381-3p to Promote Cisplatin Resistance in Nasopharyngeal Carcinoma

Li¹,

Huang²,

Yu³

et al. 2020

OTT

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“…Fibroblast growth factors (FGFs) is a heparin-binding gene family involved in various cellular and pathophysiological processes such as embryonic development, cell growth, morphogenesis, tissue repair, tumor migration and invasion (20,21,22). FGFs perform different functions by binding and activating members of the FGF receptor (FGFR) family.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential core genes in atrial fibrillation based on bioinformatics analysis

Pan

Zhang

2020

Preprint

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OBJECTIVE:Atrial fibrillation (AF) is one of the most common arrhythmias, which is caused by a number of minorring disorders caused by the heart owner's guide. It is noted in almost all organic heart disease and can also occur in non-organic heart disease,causing serious complications, such as heart failure and arterial embolism, seriously threaten people's health.Atrial fibrillation can cause serious complications, such as heart failure and arterial embolism, which seriously threaten people's health. Clinically, according to the characteristics of atrial fibrillation, atrial fibrillation is divided into paroxysmal atrial fibrillation,persistent atrial fibrillation, permanent atrial fibrillation (cannot be converted to sinus rhythm).Among them, persistent atrial fibrillation poses the greatest threat to people's health.So the main purpose of this study is to identify the differential genes in patients with permanent atrial fibrillation. MATERIALS AND METHODS:To explore potential differential genes for permanent atrial fibrillation, we analyzed three microarray datasets GSE2240 derived from the Gene Expression Omnibus (GEO) database. We used the“limma”function package of R software to screen differentially expressed genes(DEGs), and used the“pheatmap”function package to construct heatmaps for the screened differential genes.Visualization and Integration Discovery (DAVID) ,Cytoscape ,BMKcloud and String platforms were utilized for Genome Ontology (GO) analysis,Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis , PPI(protein-proteinInteraction) network analysis ,module analysis,and identification hub genes based on the selected differential genes.RESULTS:74 DEGs in total were identified, including 41 up- and 33 downregulated genes. These DEGs were mainly enriched in PI3K-Akt signaling pathway ,cGMP-PKG signaling pathway, Focal adhesion, and so on. The module analysis filtered out 12 key genes, including PRL, CREB1, AGO2, NAMPT, IGFBP2, FGF7, ANGPT2, SYT13, NRXN1, AQP4, TCEAL2, and CPLX1. 2 Hub genes were identified, including IGFBP2, and FGF7.CONCLUSIONS:IGFBP2 and FGF7 were identified as Hub genes of AF, which helped us to understand more deeply the pathophysiological mechanism of AF.

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“…Likewise, its anti-tumor role has been increasingly revealed in other malignancies such as in cervical cancer [27] and in prostate cancer [28] through the different mRNA targets. Here our study found that Second, the findings above triggered us to further explore the downstream molecules of miR-381.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-381 inhibits bladder cancer pathogenesis through directly controlling BMI1 and triggering the Rho/ROCK signaling pathway defect

Chen

Liu

Cao

et al. 2020

Preprint

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Background Emerging evidence has noted the important participation of microRNAs (miRNAs) in several human diseases including cancer control. This research was launched to probe the function of miR-381 in bladder cancer (BCs) progression. Methods Aberrantly expressed miRNAs in BCs tissues were analyzed using miRNA microarrays. miR-381 expression in the bladder and paired tumor tissues, and in BCs and normal cell lines was determined. The target relationship between miR-381 and BMI1 was predicted online and validated through a luciferase assay. Gain-of-functions of miR-381 and BMI1 were performed to identify their functions on BCs cell behaviors as well as tumor growth in vivo. Results miR-381 was poor regulated in BCs tissues and cells. A higher miR-381 level indicates a better prognosis of patients with BCs. Artificial up-regulation of miR-381 inhibited proliferation, invasion, migration, resistance to apoptosis, and tumor formation ability of BCs cells. miR-381 directly binds to BMI1 expression. Overexpression of BMI1 partially blocked the tumor suppressing roles of miR-381 in cell malignancy and tumor growth. In addition, miR-381 led to decreased RhoA phosphorylation and ROCK2 activation, which were also reversed by BMI1. Conclusion The study evidenced that miR-381 may act as a beneficiary biomarker in BCs patients. Up-regulation of miR-381 could suppress BCs development both in vivo and in vitro through BMI1 down-regulation and the Rho/ROCK inactivation.

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miR‐381‐3p restrains cervical cancer progression by downregulating FGF7

Cited by 53 publications

References 24 publications

<p>Long Non-Coding RNA DLEU1 Up-Regulates BIRC6 Expression by Competitively Sponging miR-381-3p to Promote Cisplatin Resistance in Nasopharyngeal Carcinoma</p>

<p>Long Non-Coding RNA DLEU1 Up-Regulates BIRC6 Expression by Competitively Sponging miR-381-3p to Promote Cisplatin Resistance in Nasopharyngeal Carcinoma</p>

Identification of potential core genes in atrial fibrillation based on bioinformatics analysis

MicroRNA-381 inhibits bladder cancer pathogenesis through directly controlling BMI1 and triggering the Rho/ROCK signaling pathway defect

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