Comprehensive gene and microRNA expression profiling reveals miR-206 inhibits MET in lung cancer metastasis

Chen, Qingyong; Jiao, Demin; Li, Yan; Wu, Yuquan; Hu, Huizhen; Song, Jia; Yan, Jie; Wu, Lijun; Xu, Liqun; Shi, Jianguo

doi:10.1039/c4mb00734d

Cited by 37 publications

(38 citation statements)

References 48 publications

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“…Similar findings could also be seen in cancer cell line level, including osteosarcoma [22], prostate and colon cancer [23], colorectal cancer [24], renal cancer [25], and hemangioma [26]. In our study, we have found that up-regulation of miR-424-3p was markedly capable of suppressing the migration and invasion in NSCLC cells, which was in stark contrast with Chen et al finding that miR-424-3p was significantly upregulated in high metastatic NSCLC cells via integrated bioinformatics analysis [15]. However, our findings were entirely consistent with Wu et al showed that miR-424 could suppress invasion in bladder cancer [20].…”

Section: Discussioncontrasting

confidence: 94%

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

Zhang

Zeng

Zhao

et al. 2016

Molecular Carcinogenesis

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MiR-424 has been discovered to be involved in the chemoresistance of lung cancer. However, the underlying mechanism by which miR-424 played role in chemoresistance has been unknown. Here, in our study, to investigate the role of miR-424 in non-small cell lung cancer (NSCLC), we have detected the expression of miR-424-3p and -5p in NSCLC tissues and paired normal control. Moreover, to explore the role of miR-424-3p in NSCLC cells, miR-424-3p and -5p were both re-expressed and knocked down using transient transfection with their respective mimics and inhibitors. Cell viability, migration, and invasion were evaluated using MTT, wound-healing and Transwell assays, respectively. It was found that down-regulation of miR-424-3p was pronouncedly associated with NSCLC progression and overall prognosis; and that both miR-424-3p and -5p were markedly capable of preventing the proliferation, migration, and invasion in NSCLC cells. Additionally, it is miR-424-3p but not miR-424-5p that enhances the chemo-sensitivity of NSCLC cells through targeting YAP1. Mechanistically, YAP1 was identified as down-stream target of miR-424-3p. Together, it was for the first time in our study found that it is loss of miR-424-3p not miR-424-5p that enables chemoresistance through targeting YAP1 in NSCLC, supporting that miR-424-3p could be used as therapeutic target in the curing of NSCLC with chemoresistance. © 2016 Wiley Periodicals, Inc.

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Section: Discussioncontrasting

confidence: 94%

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

Zhang

Zeng

Zhao

et al. 2016

Molecular Carcinogenesis

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“…miR‐1‐3p and miR‐206 have been identified as tumour suppressors in various human cancers, including lung cancer . Exogenous expression of these two miRNAs could significantly reduce cell motility and invasiveness .…”

Section: Resultsmentioning

confidence: 99%

“…miR-1-3p and miR-206 have been identified as tumour suppressors in various human cancers, including lung cancer. 6,12,17,18,23,24 Exogenous expression of these two miRNAs could significantly reduce cell motility and invasiveness. 25 In this study, we evaluated miR-1-3p and miR-206 expression in HGF stimulation of PC-9 and HCC827 cells.…”

Section: Pc-9 and Hcc827 Cell Lines (Both Harbouring Egfr Exon 19 Delmentioning

confidence: 99%

miR‐1‐3p and miR‐206 sensitizes HGF‐induced gefitinib‐resistant human lung cancer cells through inhibition of c‐Met signalling and EMT

Jiao

Chen

Liu

et al. 2018

J Cellular Molecular Medi

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Hepatocyte growth factor (HGF) overexpression is an important mechanism in acquired epidermal growth factor receptor (EGFR) kinase inhibitor gefitinib resistance in lung cancers with EGFR activating mutations. MiR‐1‐3p and miR‐206 act as suppressors in lung cancer proliferation and metastasis. However, whether miR‐1‐3p and miR‐206 can overcome HGF‐induced gefitinib resistance in EGFR mutant lung cancer is not clear. In this study, we showed that miR‐1‐3p and miR‐206 restored the sensitivities of lung cancer cells PC‐9 and HCC‐827 to gefitinib in present of HGF. For the mechanisms, we demonstrated that both miR‐1‐3p and miR‐206 directly target HGF receptor c‐Met in lung cancer. Knockdown of c‐Met mimicked the effects of miR‐1‐3p and miR‐206 transfections Meanwhile, c‐Met overexpression attenuated the effects of miR‐1‐3p and miR‐206 in HGF‐induced gefitinib resistance of lung cancers. Furthermore, we showed that miR‐1‐3p and miR‐206 inhibited c‐Met downstream Akt and Erk pathway and blocked HGF‐induced epithelial‐mesenchymal transition (EMT). Finally, we demonstrated that miR‐1‐3p and miR‐206 can increase gefitinib sensitivity in xenograft mouse models in vivo. Our study for the first time indicated the new function of miR‐1‐3p and miR‐206 in overcoming HGF‐induced gefitinib resistance in EGFR mutant lung cancer cell.

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“…Previous evidence has demonstrated the association between aberrant MET signaling and medulloblastoma development (33,34). Previous studies have revealed that overexpressed miR-206 may inhibit MET in lung cancer (35,36), however the function of downregulated miR-206 in medulloblastoma is unknown. SREBF1 is a transcription factor, regulating lipogenesis, which is also involved in tumorigenesis (37).…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of a microRNA expression profile in pediatric medulloblastoma

Dai

Bing

et al. 2017

Molecular Medicine Reports

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Medulloblastoma is the most common malignant brain tumor of the central nervous system among children. Medulloblastoma is an embryonal tumor, of which little is known about the pathogenesis. Several efforts have been made to understand the molecular aspects of its tumorigenic pathways; however, these are poorly understood. microRNA (miRNA), a type of non-coding short RNA, has been proven to be associated with a number of physiological processes and pathological processes of serious diseases, including brain tumors. Differentially expressed miRNAs serve an important role in numerous types of malignancy. The present study aims to define a differentially expressed set of miRNAs in medulloblastoma tumor tissue, compared with normal samples, to improve the understanding of the tumorigenesis. It was identified that 22 miRNAs were upregulated and 26 miRNAs were downregulated in the tumor tissue compared with the normal group. However, when the medulloblastoma tissue was compared with normal cerebellum tissue, 9 miRNAs were identified to be up or downregulated in the tumor samples. The differentially expressed miRNAs in the tumor tissue were identified in order to clarify the networks and pathways of tumorigenesis using Ingenuity Pathway Analysis. Subsequently, key regulatory genes associated with the development of medulloblastoma were identified, including tumor protein p53, insulin like growth factor 1 receptor, argonaute 2, mitogen-activated protein kinases 1 and 3, sirtuin 1 and Y box binding protein 1.

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Comprehensive gene and microRNA expression profiling reveals miR-206 inhibits MET in lung cancer metastasis

Cited by 37 publications

References 48 publications

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

miR‐1‐3p and miR‐206 sensitizes HGF‐induced gefitinib‐resistant human lung cancer cells through inhibition of c‐Met signalling and EMT

Comprehensive analysis of a microRNA expression profile in pediatric medulloblastoma

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