Anticancer Drug-Induced Epithelial-Mesenchymal Transition via p53/miR-34a axis in A549/ABCA3 Cells.

07:00 EST 1st January 2019 | BioPortfolio

Summary of "Anticancer Drug-Induced Epithelial-Mesenchymal Transition via p53/miR-34a axis in A549/ABCA3 Cells."

Several anticancer drugs including bleomycin (BLM) and methotrexate (MTX) cause serious lung diseases such as pulmonary fibrosis. Although evidences showing the association of epithelial-mesenchymal transition (EMT) with pulmonary fibrosis are increasing, the mechanism underlying anticancer drug-induced EMT has been poorly understood. On the other hand, miR-34a, a non-coding small RNA, has been highlighted as a key factor to regulate EMT in lung. In this study, we elucidated the role of miR-34a in anticancer drug-induced EMT using A549/ABCA3 cells as a novel type II alveolar epithelium model.


Journal Details

This article was published in the following journal.

Name: Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques
ISSN: 1482-1826
Pages: 516-524


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A transcription factor characterized by N-terminal and C-terminal CYS2-HIS2 ZINC FINGERS separated by a homeobox. It represses the expression of E-CADHERIN to induce the EPITHELIAL-MESENCHYMAL TRANSITION. It also represses PROTO-ONCOGENE PROTEINS C-BCL-6; regulates the cell type-specific expression of SODIUM-POTASSIUM-EXCHANGING ATPASE; and promotes neuronal differentiation.

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