miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells

Zhang, Junfeng; Wang, Longsheng; Mao, Shun; Liu, Mengnan; Wentao, Zhang; Zhang, Ziwei; Guo, Yadong; Huang, Bisheng; Yang, Yan; Huang, Yong; Yao, Xudong

doi:10.1159/000495273

Cited by 28 publications

(20 citation statements)

References 32 publications

(19 reference statements)

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“…It is worth mentioning that our results on GLS and GLS2 expression are in agreement with those of previous studies. For example, whereas the over-expression pattern of GLS was observed in breast, liver, and colon cancer [49,50,51,52], the under-expression pattern of this gene was noted in bladder and lung cancers [53,54]. In contrast, our results showed that GLS2 is over-expressed in bladder and lung cancers [55,56], whereas it is downregulated in liver cancer [57] which indicates that glutaminases are indeed differentially expressed in different types of human cancer.…”

Section: Resultsmentioning

confidence: 99%

Multiomics Analysis Reveals that GLS and GLS2 Differentially Modulate the Clinical Outcomes of Cancer

Saha

Islam

Abdullah-Al-Wadud

et al. 2019

JCM

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Kidney-type glutaminase (GLS) and liver-type glutaminase (GLS2) are dysregulated in many cancers, making them appealing targets for cancer therapy. However, their use as prognostic biomarkers is controversial and remains an active area of cancer research. Here, we performed a systematic multiomic analysis to determine whether glutaminases function as prognostic biomarkers in human cancers. Glutaminase expression and methylation status were assessed and their prominent functional protein partners and correlated genes were identified using various web-based bioinformatics tools. The cross-cancer relationship of glutaminases with mutations and copy number alterations was also investigated. Gene ontology (GO) and pathway analysis were performed to assess the integrated effect of glutaminases and their correlated genes on various cancers. Subsequently, the prognostic roles of GLS and GLS2 in human cancers were mined using univariate and multivariate survival analyses. GLS was frequently over-expressed in breast, esophagus, head-and-neck, and blood cancers, and was associated with a poor prognosis, whereas GLS2 overexpression implied poor overall survival in colon, blood, ovarian, and thymoma cancers. Both GLS and GLS2 play oncogenic and anti-oncogenic roles depending on the type of cancer. The varying prognostic characteristics of glutaminases suggest that GLS and GLS2 expression differentially modulate the clinical outcomes of cancers.

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Section: Resultsmentioning

confidence: 99%

Multiomics Analysis Reveals that GLS and GLS2 Differentially Modulate the Clinical Outcomes of Cancer

Saha

Islam

Abdullah-Al-Wadud

et al. 2019

JCM

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“…Moreover, miRNAs have been presented to play an essential role in migration property of various cancer cells,13 as either EMT process regulators. microRNA-1-3p (miR-1-3p) was found as a novel marker and plays as a tumor growth and migration suppressor in urinary system tumors such as bladder cancer14 and prostate cancer 15. Previous preliminary reports showed that miR-1, a homologous analog of mir-1-3p, may reflect RCC heterogeneity 16.…”

Section: Introductionmentioning

confidence: 99%

<p>miR-1-3p suppresses the epithelial-mesenchymal transition property in renal cell cancer by downregulating Fibronectin 1</p>

Liu¹,

Huang²,

Cheng³

et al. 2019

CMAR

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Purpose Renal cell cancer (RCC) is one of the primary causes of malignancy deaths all over the world. The most important cause of RCC-related mortality is metastasis. Epithelial-mesenchymal transition (EMT) plays an important role in metastasis of malignant tumors including RCC. miR-1-3p is confirmed to be decreased in many types of cancer. Nevertheless, the function of miR-1-3p in RCC metastasis and EMT process was still unclear. Materials and methods In this study, information from clinical investigation, in vitro study, and in vivo study discovered miR-1-3p expression character and its status in RCC. The character of miR-1-3p in invasive and metastatic properties in vitro and in vivo was also inspected in RCC cells and xenograft tumor model, and expression levels of EMT markers were evaluated in RCC cells and tissues. Results miR-1-3p was proved to be decreased in RCC cell lines and tissues compared with normal renal cells and tissues. miR-1-3p expression level in RCC tissues was closely related with capsulation, lymph node metastasis, and vascular invasion. miR-1-3p was found to be able to block the EMT process in A498 and CAKI-1 RCC cells and tumors. Luciferase reporter assay and expression level rescue assays were employed to reveal that miR-1-3p inhibited the invasion and migration property of RCC cells by directly targeting Fibronectin 1. Upregulation of Fibronectin 1 partially reversed the suppressive effect of miR-1-3p on EMT process. Conclusion In brief, this study has verified that miR-1-3p blocked the EMT process of RCC cells by reducing Fibronectin 1 expression. miR-1-3p/Fibronectin 1 axis may be considered as a new target for drug development of RCC.

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“…Then, miRNA-mRNA regulatory network revealed that miR-1-3p, miR-10a-3p, miR-10a-5p and miR-133a-3p had rich external connections, while miR-99b-5p have few external connections. miR-1-3p acted as a tumor suppressor in acute myeloid leukemia [28], bladder cancer [29], non-small-cell lung cancer [30], hepatocellular carcinoma [31] and so on. Zhi Y et al reported that high miR-10a-5p expression was associated with poorer overall survival of AML patients [32].…”

Section: Discussionmentioning

confidence: 99%

Identification of the key genes and microRNAs in adult acute myeloid leukemia with FLT3 mutation by bioinformatics analysis

Chen¹,

Chen²,

Zhu³

et al. 2020

Int. J. Med. Sci.

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Background: Associated with poor prognosis, FMS-like tyrosine kinase 3 (FLT3) mutation appeared frequently in acute myeloid leukemia (AML). Herein, we aimed to identify the key genes and miRNAs involved in adult AML with FLT3 mutation and find possible therapeutic targets for improving treatment. Materials: Gene and miRNA expression data and survival profiles were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. EdgeR of R platform was applied to identify the differentially expressed genes and miRNAs (DEGs, DE-miRNAs). Gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Metascape and DAVID. And protein-protein interaction network, miRNA-mRNA regulatory network and clustering modules analyses were performed by STRING database and Cytoscape software. Results: Survival analysis showed FLT3 mutation led to adverse outcome in AML. 24 DE-miRNAs (6 upregulated, 18 downregulated) and 250 DEGs (54 upregulated, 196 downregulated) were identified. Five miRNAs had prognostic value and the results matched their expression levels (miR-1-3p, miR-10a-3p, miR-10a-5p, miR-133a-3p and miR-99b-5p). GO analysis showed DEGs were enriched in skeletal system development, blood vessel development, cartilage development, tissue morphogenesis, cartilage morphogenesis, cell morphogenesis involved in differentiation, response to growth factor, cell-substrate adhesion and so on. The KEGG analysis showed DEGs were enriched in PI3K-Akt signaling pathway, ECM-receptor interaction and focal adhesion. Seven genes (LAMC1, COL3A1, APOB, COL1A2, APP, SPP1 and FSTL1) were simultaneously identified by hub gene analysis and module analysis. SLC14A1, ARHGAP5 and PIK3CA, the target genes of miR-10a-3p, resulted in poor prognosis. Conclusion: Our study successfully identified molecular markers, processes and pathways affected by FLT3 mutation in AML. Furthermore, miR-10a-3p, a novel oncogene, might involve in the development of FLT3 mutation adult AML by targeting SLC14A1, ARHGAP5 and PIK3CA.

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miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells

Cited by 28 publications

References 32 publications

Multiomics Analysis Reveals that GLS and GLS2 Differentially Modulate the Clinical Outcomes of Cancer

Multiomics Analysis Reveals that GLS and GLS2 Differentially Modulate the Clinical Outcomes of Cancer

<p>miR-1-3p suppresses the epithelial-mesenchymal transition property in renal cell cancer by downregulating Fibronectin 1</p>

Identification of the key genes and microRNAs in adult acute myeloid leukemia with FLT3 mutation by bioinformatics analysis

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