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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ADAM9 Up-regulates N-Cadherin via MiR-218 Suppression in Lung Adenocarcinoma Cells [miRNA]

ABSTRACT: Lung cancer is the leading cause of cancer death worldwide. Brain metastasis is a major cause of morbidity and mortality in lung cancer. CDH2 (N-cadherin, a mesenchymal marker in epithelial-mesenchymal transition) and ADAM9 (a member of type I transmembrane proteins) have been reported relating to lung cancer brain metastasis, however, it is still not clear whether any interaction between them to mediate lung cancer brain metastasis. Since microRNAs were discovered to regulate many biological functions and disease processes (e.g., cancer) by down-regulating their target genes, microRNA microarrays were used to identify ADAM9 regulated miRNAs that target CDH2 in aggressive lung cancer cells. Luciferase assays and immunoblotting proved that CDH2 was a target gene of miR-218. The expression of miR-218 was generated from pri-mir-218-1, located in SLIT2, in low invasive lung adenocarcinoma while it was inhibited in aggressive lung adenocarcinoma. Down-regulation of ADAM9 could up-regulate SLIT2 and miR-218, thus down-regulate CDH2 expression. This study elucidated the mechanism of ADAM9 activating CDH2 may be due to release the inhibition of miR-218 on CDH2 in lung adenocarcinoma. For each of the cell lines bm#2, bm#7, and F4, one microarray was analyzed.

ORGANISM(S): Homo sapiens

SUBMITTER: Mong-Hsun Tsai

PROVIDER: E-GEOD-51833 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ADAM9 Up-regulates N-Cadherin via MiR-218 Suppression in Lung Adenocarcinoma Cells [mRNA]

Project description:Lung cancer is the leading cause of cancer death worldwide. Brain metastasis is a major cause of morbidity and mortality in lung cancer. CDH2 (N-cadherin, a mesenchymal marker in epithelial-mesenchymal transition) and ADAM9 (a member of type I transmembrane proteins) have been reported relating to lung cancer brain metastasis, however, it is still not clear whether any interaction between them to mediate lung cancer brain metastasis. Since microRNAs were discovered to regulate many biological functions and disease processes (e.g., cancer) by down-regulating their target genes, microRNA microarrays were used to identify ADAM9 regulated miRNAs that target CDH2 in aggressive lung cancer cells. Luciferase assays and immunoblotting proved that CDH2 was a target gene of miR-218. The expression of miR-218 was generated from pri-mir-218-1, located in SLIT2, in low invasive lung adenocarcinoma while it was inhibited in aggressive lung adenocarcinoma. Down-regulation of ADAM9 could up-regulate SLIT2 and miR-218, thus down-regulate CDH2 expression. This study elucidated the mechanism of ADAM9 activating CDH2 may be due to release the inhibition of miR-218 on CDH2 in lung adenocarcinoma. For each of the cell lines bm#2, bm#7, and F4, one microarray was analyzed.

2016-07-03 | E-GEOD-52050 | biostudies-arrayexpress

ADAM9 Up-regulates N-Cadherin via MiR-218 Suppression in Lung Adenocarcinoma Cells [mRNA]

2016-01-01 | GSE52050 | GEO

ADAM9 Up-regulates N-Cadherin via MiR-218 Suppression in Lung Adenocarcinoma Cells [miRNA]

2016-01-01 | GSE51833 | GEO

ADAM9 Up-regulates N-Cadherin via MiR-218 Suppression in Lung Adenocarcinoma Cells

Project description:Identification of miRNAs that differentially expressed in brain metastatic cells and were predicted to target CDH2. To investigate which miRNAs could regulate CDH2 expression in brain-metastatic lung cancer cells, we examined the miRNA expression profiles in brain-metastatic lung cancer cells and their parental cells using Illumina miRNA microarray. By comparing the endogenous expression of all miRNAs, 146 miRNAs were selected by 2-fold changes in brain-metastatic lung cancer cells. Furthermore, we used several algorithms in miRSystem to predict which miRNA whose target gene was CDH2. There were 44 miRNAs that were predicted to target CDH2. In total, we identified nine miRNAs whose target gene was CDH2 and whose expression was significantly different between the highly metastatic cells and their parental cells (Fig. 2A). Among these miRNAs, four miRNAs were found to be down-regulated and five miRNAs were up-regulated in brain-metastatic lung cancer cells (Fig. 2B).

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Project description:Receptor tyrosine kinase pathway signalings plays a central role in the growth and progression of glioblastoma, a highly aggressive group of brain tumors. We recently reported that miR-218 repression, an essentially uniform feature of human GBM, directly promotes RTK hyperactivation by increasing the expression of key positive signaling effectors, including EGFR, PLCr1, PIK3CA and ARAF. However, enhanced RTK signaling is known to activate compensatory inhibitory feedback mechanisms in both normal and cancer cells. We demonstrate here that miR-218 repression in GBM cells also increases the abundance of additional up stream and downstream signaling mediators, including PDGFRa, RSK2, and S6K1, which collectively funciton to alleviate inhibitory RTK feedback regulation. In turn, RTK signaling suppresses miR-218 expression via STAT3, which binds to the miR-218 locus, along with BCLAF1, to repress its expression. These data identify novel interacting feedback loops by which miR-218 repression promotes increased RTK signaling in high-grade gliomas.

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