Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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MicroRNA-dependent regulation of transcription in lung cancer

ABSTRACT: The objective is to establish robust transcriptional regulation differences between squamous cell carcinoma (SCC) and adenocarcinoma (ADC) by studying miRNA and concurrent transcriptional profiles. This series represents the miRNA profiles only (not mRNA). The related mRNA data is in Series GSE42998. The present study was performed in 44 tumour samples following surgical resection for clinical early stage NSCLC (20 lung adenocarcinoma and 24 squamous cell lung cancer). Mature human miRNA expression was detected and quantified using the TaqMan® Low Density Arrays (TLDA). The Human MicroRNA Card Set v2.0 array is a two card set containing a total of 384 TaqMan® MicroRNA Assays per card to enable accurate quantification of 667 human microRNAs, all catalogued in the miRBase database.Expression of target miRNAs was normalized in relation to the expression of RNU48. Cycle threshold (Ct) values were calculated using the SDS software v.2.3 using automatic baseline settings and a threshold of 0.2. Relative quantification of miRNA expression was calculated by the 2−ΔCt method (Applied Biosystems user bulletin no. 2 (P/N 4303859)).

ORGANISM(S): Homo sapiens

SUBMITTER: Sonia Molina-Pinelo

PROVIDER: E-GEOD-43000 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Epithelial-mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non-small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA) -related mechanisms underlying EMT followed by acquired resistance to epidermal growth factor receptor tyrosine-kinase inhibitor (EGFR-TKI) in NSCLC. MiRNA expression profiles were examined before and after transforming growth factor-beta1 (TGF-M-NM-21) exposure in four human adenocarcinoma cell lines with or without EMT. Correlation between expressions of EMT-related miRNAs and resistance to EGFR-TKI gefitinib was evaluated. MiRNA array and quantitative RT-PCR revealed that TGF-M-NM-21 significantly induced overexpression of miR-134, miR-487b, and miR-655, which belong to the same cluster located on chromosome 14q32, in lung adenocarcinoma cells with EMT. MAGI2 (membrane-associated guanylate kinase, WW and PDZ domain-containing protein 2), a predicted target of these miRNAs and a scaffold protein required for PTEN (phosphatase and tensin homolog), was diminished in A549 cells with EMT after the TGF-M-NM-21 stimulation. Overexpression of miR-134 and miR-487b promoted the EMT phenomenon and affected the drug resistance to gefitinib, whereas knockdown of these miRNAs inhibited the EMT process and reversed TGF-M-NM-21-induced resistance to gefitinib. Our study demonstrated that the miR-134/487b/655 cluster contributed to the TGF-M-NM-21-induced EMT phenomenon and affected the resistance to gefitinib by directly targeting MAGI2, whose suppression subsequently caused loss of PTEN stability in lung cancer cells. The miR-134/miR-487b/miR-655 cluster may be new therapeutic targets in advanced lung adenocarcinoma patients, depending on the EMT phenomenon. miRNA expression profiles before and after TGF-M-NM-21 exposure were assessed in the four lung adenocarcinoma cell lines, A549, LC2/ad, PC3, and, PC9 by TaqMan miRNA arrays. Relative ratios of miRNAs in cells after TGF-M-NM-21 exposure were calculated when compared with the cells before TGF-M-NM-21 exposure.

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MicroRNA-dependent regulation of transcription in lung cancer

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