A two-miRNA signature (miR-33a-5p and miR-128-3p) in whole blood as potential biomarker for early diagnosis of lung cancer

Pan, Jinchang; Zhou, Chengwei; Zhao, Xiaodong; He, Jiamin; Tian, Hui; Shen, Weiyu; Han, Ying; Fang, Shuai; Meng, Xiaoxiao; Jin, Xiaofeng; Gong, Zhaohui

doi:10.1038/s41598-018-35139-3

Cited by 79 publications

(72 citation statements)

References 41 publications

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“…Moreover, the deficit or excess of miRNAs have been associated with several human diseases, such as, myocardial infarction and different types of cancer [12]. miRNAs reside not only inside cells, but also in a variety of biofluids [13][14][15], which has suggested they could be used as noninvasive disease biomarkers or therapies [16,17,18,10].…”

Section: Resultsmentioning

confidence: 99%

Unification of miRNA and isomiR research: the mirGFF3 format and the mirtop API

Desvignes

Loher

Eilbeck

et al. 2018

Preprint

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Background:MicroRNAs (miRNAs) are small RNA molecules (~22 nucleotide long) involved in posttranscriptional gene regulation. Advances in high-throughput sequencing technologies led to the discovery of isomiRs, which are miRNA sequence variants. While many miRNA-seq analysis tools exist, a lack of consensus on miRNA/isomiR analyses exists, and the resulting diversity of output formats hinders accurate comparisons between tools and precludes data sharing and the development of common downstream analysis methods. Conclusions:Collectively a comprehensive isomiR categorization system, along with the accompanying mirGFF3 and mirtop API provide a complete solution for the standardization of miRNA and isomiR analysis, enabling data sharing, reporting, comparative analyses, and benchmarking, while promoting the development of common miRNA methods focusing on downstream steps to miRNA detection, annotation, and quantification.

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Section: Resultsmentioning

confidence: 99%

Unification of miRNA and isomiR research: the mirGFF3 format and the mirtop API

Desvignes

Loher

Eilbeck

et al. 2018

Preprint

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“…It was reported that miR-33a was downregulated in a variety of cancers, and ectopic expression of miR-33a suppressed multiple malignant behaviors [15][16][17][18]. miR-33a can suppress epithelial-mesenchymal transition and metastasis in non-small cell lung cancer, and its expression in the blood of lung cancer patients was lower than that in healthy controls; thus, it could be regarded as a tumor suppressor and a novel biomarker for the diagnosis of lung cancer [15,35]. It also targets ST8SIA1 to suppress colorectal cancer progression [36] and targets HIF-1α to inhibit melanoma cell growth and mobility [37].…”

Section: Discussionmentioning

confidence: 99%

“…and metastasis [12,13]. MiR-33a downregulation has been associated with cancer cell proliferation, mobility and chemotherapy sensitivity in various cancers, including lung cancer [14,15], prostate cancer [16] and BC [17,18], which suggested that it functions as a tumor suppressor. MiR-33a was upregulated after treatment with chidamide in TNBC and suppressed glycolysis by targeting LDHA [19].…”

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confidence: 99%

MiR-33a functions as a tumor suppressor in triple-negative breast cancer by targeting EZH2

et al. 2020

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Background: Increasing reports have confirmed that microRNAs play an important role in breast cancer progression, particularly in triple-negative breast cancer (TNBC). The aim of our study was to investigate the role of miR-33a in TNBC progression.Methods: PCR assays were performed to detect miR-33a and EZH2 expression in TNBC tissues, adjacent nontumor tissues and cell lines. Western blot, CCK8, Transwell, cell colony formation and EdU cell proliferation, cell cycle analysis and luciferase reporter assays were used to determine the regulation of miR-33a/EZH2 in TNBC progression.Results: MiR-33a was significantly downregulated in TNBC tissues and cell lines. MiR-33a overexpression in TNBC cells significantly inhibited cell growth and mobility and induced G1 cell cycle arrest. The luciferase reporter assay revealed that EZH2 is a direct target of miR-33a and that it was upregulated in TNBC tissues and cell lines. There was a negative correlation between miR-33a and EZH2 expression in TNBC tissues. EZH2 knockdown exerted similar inhibitory effects, while ectopic expression of EZH2 showed suppressive effects on malignant behaviors induced by miR-33a overexpression in TNBC cells. Conclusions:These findings revealed that miR-33a is a tumor-suppressive miRNA in TNBC and can inhibit proliferation and mobility and induce G1 cell cycle arrest by directly targeting EZH2.

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“…As oncogenes or tumor suppressor genes, miRNAs play a regulatory role in a variety of cancers, including lung cancer. Recently, miR-1284, miR-17-92, miR-33a-5p and miR-128-3p have been found to take important part in lung cancer [9][10][11]. miR-16-5p is involved in the development of gastric cancer and chordoma [12,13], and its research in lung cancer is still unclear.…”

Section: Discussionmentioning

confidence: 99%

The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3

Liu

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Objective: To study the effect of miR-16-5p on lung cancer cell injury and apoptosis, and its mechanism. Methods: LPS induced lung cancer cell A549 injury; qRT-PCR method was applied to detect the expression of miR-16-5p and CXCR3 in A549 cells. Con (without LPS treatment), LPS þ miR-NC group (transfected negative control samples), LPS þ miR-16-5p group (transfected miR-16-5p mimics); LPS þ si-NC group (transfected negative control samples), LPS þ si-CXCR3 group (transfected si-CXCR3); LPS þ miR-16-5p þ pcDNA3.1 group (co-transfected miR-16-5p mimics and pcDNA3.1), LPS þ miR-16-5p þ pcDNA3.1-CXCR3 group (co-transfected miR-16-5p mimics and pcDNA3.1-CXCR3) were transfected into A549 cells by liposome method. Western blot was used to detect protein expression of CXCR3, IL-6 and TNF-a in A549 cells; apoptosis of A549 cells was detected by flow cytometry. Results: Compared with the control group, the expression of miR-16-5p mRNA was significantly decreased in A549 cells in LPS group, and the mRNA and protein expression of CXCR3 were significantly increased (p < .05). Overexpression of miR-16-5p and knockdown of CXCR3 both can downregulated protein expression of IL-6 and TNF-a, and up-regulated apoptosis in LPS-induced A549 cell; CXCR3 is a target of miR-16-5p. Overexpression of CXCR3 rescued the protective effect of miR-16-5p on LPS-induced A549 cell injury. Conclusion: miR-16-5p can protect LPS-induced A549 cell injury, and its mechanism may be related to the targeted regulation of CXCR3, which could provide a new target for targeted therapy of lung cancer.

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A two-miRNA signature (miR-33a-5p and miR-128-3p) in whole blood as potential biomarker for early diagnosis of lung cancer

Cited by 79 publications

References 41 publications

Unification of miRNA and isomiR research: the mirGFF3 format and the mirtop API

Unification of miRNA and isomiR research: the mirGFF3 format and the mirtop API

MiR-33a functions as a tumor suppressor in triple-negative breast cancer by targeting EZH2

The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3

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