An achaete-scute homologue essential for neuroendocrine differentiation in the lung View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-04-24

AUTHORS

Michael Borges, R. Ilona Linnoila, Helgi J. K. van de Velde, Herbert Chen, Barry D. Nelkin, Mack Mabry, Stephen B. Baylin, Douglas W. Ball

ABSTRACT

In Drosophila and in vertebrates, the achaete-scute family of basic helix–loop–helix transcription factors plays a critical developmental role in neuronal commitment and differentiation1–6. Relatively little is known, however, about the transcriptional control of neural features in cells outside a neuronal context. A minority of normal bronchial epithelial cells and many lung cancers, especially small-cell lung cancer, exhibit a neuroendocrine phenotype that may reflect a common precursor cell population7–11. We show here that human achaete-scute homologue-–1 (hASH1) is selectively expressed in normal fetal pulmonary neuroendocrine cells, as well as in the diverse range of lung cancers with neuroendocrine features. Strikingly, newborn mice bearing a disruption of the ASH1 gene have no detectable pulmonary neuroendocrine cells. Depletion of this transcription factor from lung cancer cells by antisense oligonucleotides results in a significant decrease in the expression of neuroendrocrine markers. Thus, a homologue of Drosophila neural fate determination genes seems to be necessary for progression of lung epithelial cells through a neuroendocrine differentiation pathway that is a feature of small-cell lung cancer, the most lethal form of human lung cancer. More... »

PAGES

852-855

Journal

TITLE

Nature

ISSUE

6627

VOLUME

386

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/386852a0

DOI

http://dx.doi.org/10.1038/386852a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1004814255

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9126746


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