Integrated microRNA and mRNA signatures in peripheral blood lymphocytes of familial epithelial ovarian cancer

Dou, Yun-De; Huang, Tao; Wang, Qun; Shu, Xin; Zhao, Shigang; Li, Lei; Liu, Tao; Lü, Gang; Chan, Wai‐Yee; Liu, Hongbin

doi:10.1016/j.bbrc.2018.01.023

Cited by 5 publications

(3 citation statements)

References 56 publications

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“…Several studies have demonstrated that miR-34b was reduced or lost in a number of cancers, including breast cancer, epithelial ovarian cancer and Gastric Cancer [12][13][14]. The association between a polymorphism in miR-34b and risk of cancer was also reported in independent studies and metaanalyses [15,16].…”

Section: Introductionmentioning

confidence: 93%

MiR-34b regulates cervical cancer cell proliferation and apoptosis

Zhi-min

Zhang

Xie

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Objectives: MiR-34b is a tumour suppressor in different kinds of carcinomas. This study investigated the role of miR-34b in proliferation and apoptosis of cervical cancer. Materials and methods: The expression of miR-34b in 60 cervical cancer patients were quantified by RT-PCR and correlated with their clinicopathological parameters. Besides, there is a significant reverse relationship between miR-43b and TGF-β1 expression in tumour tissues. Cell proliferation and apoptosis was detected by CCK-8 assays and flow cytometry in cell lines transfected with miR-34b mimics. Western blotting, quantitative reverse transcription-PCR (RT-PCR) and luciferase assays were conducted to analyze the regulation of TGF-β1 by miR-34b in cell lines. Results: Here, we found expression of miR-34b to be downregulated in cervical cancer in comparison with the adjacent normal tissues. Expression levels of miR-34b were associated with enhanced malignant potential, such as tumour stage and stromal invasion. The overexpression of miR-34b potently suppressed cell proliferation and induced the apoptosis of cell lines. Conclusions: MiR-34b and TGF-β1 contribute to cervical cancer cell proliferation and apoptosis and are potential targets for cervical cancer therapeutics.

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Section: Introductionmentioning

confidence: 93%

MiR-34b regulates cervical cancer cell proliferation and apoptosis

Zhi-min

Zhang

Xie

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Stated thus, a hypothesis can be made that miRNAs may participate in OC metastasis via modulating their target genes. Notably, emerging evidence has demonstrated the importance of the miRNA-mRNA interplay in the pathogenesis and metastasis of OC [12,13]. Therefore, differentially expressed miRNAs and mRNAs were screened from primary and metastatic tissues of OC using highthroughput sequencing technique.…”

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confidence: 99%

High-throughput sequencing identification of differentially expressed microRNAs in metastatic ovarian cancer with experimental validations

Zhang

2020

Cancer Cell Int

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Background Ovarian cancer (OC) is a common gynecological cancer and characterized by high metastatic potential. MicroRNAs (miRNAs, miRs) have the promise to be harnessed as prognostic and therapeutic biomarkers for OC. Herein, we sought to identify differentially expressed miRNAs and mRNAs in metastatic OC, and to validate them with functional experiments. Methods Differentially expressed miRNAs and mRNAs were screened from six pairs of primary OC tissues and metastatic tissues using a miRStar™ Human Cancer Focus miRNA and Target mRNA PCR Array. Then, gene expression profiling results were verified by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot assays. The binding affinity between miR-7-5p and TGFβ2 was validated by dual-luciferase reporter assay. Expression of miR-7-5p and TGFβ2 was manipulated to assess their roles in malignant phenotypes of highly metastatic HO-8910PM cells. Results MiRNA profiling and sequencing identified 12 miRNAs and 10 mRNAs that were differentially expressed in metastatic tissues. Gene ontology and Pathway analyses determined that 3 differentially expressed mRNAs (ITGB3, TGFβ2 and TNC) were related to OC metastasis. The results of RT-qPCR confirmed that the decrease of miR-7-5p was most significant in OC metastasis, while TGFβ2 was up-regulated in OC metastasis. Moreover, miR-7-5p targeted and negatively regulated TGFβ2. MiR-7-5p overexpression accelerated HO-8910PM cell viability and invasion, and TGFβ2 overexpression reversed the results. Meanwhile, simultaneous miR-7-5p and TGFβ2 overexpression rescued the cell activities. Conclusions This study characterizes differentially expressed miRNAs and mRNAs in metastatic OC, where miR-7-5p and its downstream target were most closely associated with metastatic OC. Overexpression of miR-7-5p targets and inhibits TGFβ2 expression, thereby inhibiting the growth and metastasis of OC.

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“…In other words, any changes in both chromosomes and the genes as amplification defects, translocation or deletion can result in abnormal changes in genomic miRNA copy numbers leading to the changes in normal regulatory functions of miRNAs [ 23 ]. Genome-wide association studies could discover many genes encoding miRNAs in cancer-related genomic regions that might be oncogene or have tumor-suppressing role [ 24 , 25 ]. As initially described by Teague in 2010, miR-125a and miR-125b are tumor suppressor miRNAs that are up-regulated in the endometriotic lesions and involve in controlling cell migration and invasion.…”

Section: Introductionmentioning

confidence: 99%

A Systematic Review and Bioinformatics Study on Genes and micro-RNAs Involving the Transformation of Endometriosis into Ovarian Cancer

Sheikhvatan

Chaichian

Moazzami

2020

MIRNA

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Background: Along with the description of tumorigenesis processes in endometriosisrelated ovarian cancer, identifying dysregulated miRNAs, the target genes of these miRNAs, and the processes abnormally affected by dysregulated miRNAs is essential, which was our goal. Methods: Two reviewers individually evaluated the articles which collected relevant information including genes and miRNAs involved in the transformation of endometriosis into ovarian cancer. To assess the mature sequence of miRNAs and also their chromosomal positions, miRPathDB software was employed. To determine the main target gene predicted for each considered miRNAs, the TargetScanS Web server was applied. The interaction of each gene with other genes associated with endometrial- related ovarian cancer was determined by GeneMANIA software. Finally, to design integrated model of miRNAs-targeted genes interaction network, the Cytoscape software was used. Results: The final number of studies available for analysis was 6 manuscripts including 22 miRNAs described as involved in the transformation of endometriosis into different subtypes of ovarian cancers (14 miRNAs up-regulated and 8 miRNAs down-regulated). Three miRNAs of miR-141 (upregulated), miR-205 (down-regulated), and miR-125b (down-regulated) were revealed as the originator for genetic interactions leading to carcinogenesis. We could show some common loops and pathways including uncontrolled cell proliferation and abnormal apoptosis (mediated by PTEN gene induced by miR-21 and miR-214), and disaggregation and epithelialization (mediated by ZEB1 and ZEB2 genes induced by miR-200). Conclusions: According to our analysis, up-regulation of miR-141 and down-regulation of miR-205 and miR-125b have a central role in transforming endometriosis to ovarian cancer.

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Integrated microRNA and mRNA signatures in peripheral blood lymphocytes of familial epithelial ovarian cancer

Cited by 5 publications

References 56 publications

MiR-34b regulates cervical cancer cell proliferation and apoptosis

MiR-34b regulates cervical cancer cell proliferation and apoptosis

High-throughput sequencing identification of differentially expressed microRNAs in metastatic ovarian cancer with experimental validations

A Systematic Review and Bioinformatics Study on Genes and micro-RNAs Involving the Transformation of Endometriosis into Ovarian Cancer

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