Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

ASH1_A549 vs. vector control_A549

ABSTRACT: We performed genome-wide expression profiling of miRNAs in order to search for those significantly affected by ASH1 transduction in a lung cancer cell line. Microarray analysis was?conducted to examine miRNA expression profiles using a Human miRNA Microarray, pre-commercial version 6.0 (Agilent) with 470 miRNA probes, according to the manufacturer’s instructions. A549 cells were infected with an ASH1-expressing or empty lentivirus and harvested 4 days later.

ORGANISM(S): Homo sapiens

SUBMITTER: Osada Hirotaka

PROVIDER: E-GEOD-31565 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

miR-375 is activated by ASH1 and inhibits YAP1 in a lineage-dependent manner in lung cancer.

Nishikawa Eri E Osada Hirotaka H Okazaki Yasumasa Y Arima Chinatsu C Tomida Shuta S Tatematsu Yoshio Y Taguchi Ayumu A Shimada Yukako Y Yanagisawa Kiyoshi K Yatabe Yasushi Y Toyokuni Shinya S Sekido Yoshitaka Y Takahashi Takashi T

Cancer research 20110819 19

Lung cancers with neuroendocrine (NE) features are often very aggressive but the underlying molecular mechanisms remain elusive. The transcription factor ASH1/ASCL1 is a master regulator of pulmonary NE cell development that is involved in the pathogenesis of lung cancers with NE features (NE-lung cancers). Here we report the definition of the microRNA miR-375 as a key downstream effector of ASH1 function in NE-lung cancer cells. miR-375 was markedly induced by ASH1 in lung cancer cells where it ...[more]

PMID: 21856745

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Project description:Accumulation of genetic and epigenetic changes alters regulation of a web of interconnected genes including miRNAs, which confer hallmark capabilities and characteristic cancer features. In this study, the miRNA and mRNA expression profiles of 126 non-small cell lung cancer specimens were analyzed, with special attention given to the diversity of lung adenocarcinomas. Of those, 76 adenocarcinomas were classified into two major subtypes, developing lung-like and adult lung-like, based on their distinctive miRNA expression profiles resembling those of either developing or adult lungs, respectively. A systems biology-based approach using a Bayesian network and nonparametric regression was employed to estimate the gene regulatory circuitry functioning in patient tumors in order to identify subnetworks enriched for genes with differential expression between the two major subtypes. miR-30d and miR-195, identified as hub genes in such subnetworks, had lower levels of expression in the developing lung-like subtype, while introduction of miR-30d or miR-195 into the lung cancer cell lines evoked shifts of mRNA expression profiles towards the adult lung-like subtype. Conversely, the influence of miR-30d and miR-195 was significantly different between the developing lung- and adult lung-like subtypes in our analysis of the patient dataset. In addition, RRM2, a child gene of the miR-30d-centered subnetwork, was found to be a direct target of miR-30d. Together, our findings reveal the existence of two miRNA expression profile-defined lung adenocarcinoma subtypes with distinctive clinicopathologic features and also suggest the usefulness of a systems biology-based approach to gain insight into the altered regulatory circuitry involved in cancer development. Microarray analysis was conducted to examine miRNA expression profiles using a Human miRNA Microarray, pre-commercial version 6.0 (Agilent) with 470 miRNA probes, according to the manufacturer’s instructions

Dataset Information

ASH1_A549 vs. vector control_A549

Publications

miR-375 is activated by ASH1 and inhibits YAP1 in a lineage-dependent manner in lung cancer.

Similar Datasets

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