The BTB-zinc finger transcription factor Abrupt acts as an epithelial oncogene in Drosophila through maintaining a progenitor-like cell state

ABSTRACT: The capacity of tumor cells to maintain continual overgrowth potential has been linked to the commandeering of normal self-renewal pathways. Using an epithelial cancer model in Drosophila we carried out an overexpression screen for oncogenes capable of cooperating with the loss of the epithelial apico-basal cell polarity regulator, scribbled, and identified the cell fate regulator, Abrupt, a BTB-zinc finger protein. Abrupt overexpression alone is insufficient to transform cells, but in cooperation with scrib loss of function, Abrupt promotes the formation of massive tumors in the eye/antennal disc. The steroid hormone receptor coactivator, Taiman (SRC3/AIB1), is known to associate with Abrupt, and Taiman overexpression also drives tumor formation in cooperation with the loss of Scribbled.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Enrique Blanco 

PROVIDER: E-GEOD-42928 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress