CEBPG induces epithelial-mesenchymal transition and facilitates DNA double-strand break repair in lung adenocarcinoma cells

Although core EMT-TFs are well characterized, much remains unknown of context-dependent EMT-TFs restricted to specific tissues or cell types. Here, we identified CEBPG as a novel inducer of EMT in lung adenocarcinoma cells by examining regions of extensive histone H3 lysine 4 trimethylation occupancy that are often a hallmark of cellular identity.

Transiently induced during TGF--driven EMT, ectopic CEBPG induced mesenchymal-like morphologies and gene expression, while its RNAi knockdown attenuated EMT. Domain mapping analysis of CEBPG demonstrated the indispensability of the leucine zipper domain, rather than the DNA binding domain, suggesting the involvement of protein partners. Co-immunoprecipitation and mass spectrometry identified interactions of CEBPG with non-homologous end joining (NHEJ) factors and CEBPB.