Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

EMT-induced stemness and tumorigenicity are fueled by an oncogenic EGF/Ras pathway

ABSTRACT: Pre-EMT GIF14 cells treated with TGF-M-NM-21 Total RNA obtained from isolated GIF-14 cells from untreated and TGF-M-NM-21-treated sample

ORGANISM(S): Mus musculus

SUBMITTER: Tuan Zea Tan

PROVIDER: E-GEOD-44055 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

EMT-induced stemness and tumorigenicity are fueled by the EGFR/Ras pathway.

Voon Dominic Chih-Cheng DC Wang Huajing H Koo Jason Kin Wai JK Chai Juin Hsien JH Hor Yit Teng YT Tan Tuan Zea TZ Chu Yeh-Shiu YS Mori Seiichi S Ito Yoshiaki Y

PloS one 20130812 8

Recent studies have revealed that differentiated epithelial cells would acquire stem cell-like and tumorigenic properties following an Epithelial-Mesenchymal Transition (EMT). However, the signaling pathways that participate in this novel mechanism of tumorigenesis have not been fully characterized. In Runx3 (-/-) p53 (-/-) murine gastric epithelial (GIF-14) cells, EMT-induced plasticity is reflected in the expression of the embryonal proto-oncogene Hmga2 and Lgr5, an exclusive gastrointestinal ...[more]

PMID: 23950932

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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.

Dataset Information

EMT-induced stemness and tumorigenicity are fueled by an oncogenic EGF/Ras pathway

Publications

EMT-induced stemness and tumorigenicity are fueled by the EGFR/Ras pathway.

Similar Datasets

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