• Detection of phenotype-specific therapeutic vulnerabilities in breast cells using a CRISPR loss-of-function screen 

      Barkovskaya, Anna; Goodwin, Craig; Seip, Kotryna; Hilmarsdòttir, Bylgja; Pettersen, Solveig; Stalnecker, Clint; Engebraaten, Olav; Briem, Eirikur; Der, Channing J; Moestue, Siver Andreas; Guðjónsson, Þórarinn; Mælandsmo, Gunhild Mari; Prasmickaite, Lina (Journal article; Tidsskriftartikkel; Peer reviewed, 2021-03-24)
      Cellular phenotype plasticity between the epithelial and mesenchymal states has been linked to metastasis and heterogeneous responses to cancer therapy, and remains a challenge for the treatment of triple-negative breast cancer (TNBC). Here, we used isogenic human breast epithelial cell lines, D492 and D492M, representing the epithelial and mesenchymal phenotypes, respectively. We employed a CRISPR-Cas9 ...
    • Fibroblast-induced switching to the mesenchymal-like phenotype and PI3K/mTOR signaling protects melanoma cells from BRAF inhibitors 

      Vasiliauskaite, Kotryna; Fleten, Karianne Giller; Barkovskaya, Anna; Nygaard, Vigdis; Haugen, Mads Haugland; Engesæter, Birgit Øvstebø; Mælandsmo, Gunhild; Prasmickaite, Lina (Journal article; Tidsskriftartikkel; Peer reviewed, 2016)
      The knowledge on how tumor-associated stroma influences efficacy of anti-cancer therapy just started to emerge. Here we show that lung fibroblasts reduce melanoma sensitivity to the BRAF inhibitor (BRAFi) vemurafenib only if the two cell types are in close proximity. In the presence of fibroblasts, the adjacent melanoma cells acquire de-differentiated mesenchymal-like phenotype. Upon treatment with ...
    • Metabolic re-wiring of isogenic breast epithelial cell lines following epithelial to mesenchymal transition 

      Haldorsson, Skarphedinn; Rohatgi, Neha; Magnusdottir, Manuela; Choudhary, Kumari; Gudjónsson, Thorarinn; Knutsen, Erik; Barkovskaya, Anna; Hilmarsdòttir, Bylgja; Perander, Maria; Mælandsmo, Gunhild; Gudmundsson, Steinn; Rolfsson, Ottar (Journal article; Tidsskriftartikkel; Peer reviewed, 2017-03-18)
      Epithelial to mesenchymal transition (EMT) has implications in tumor progression and metastasis. Metabolic alterations have been described in cancer development but studies focused on the metabolic re-wiring that takes place during EMT are still limited. We performed metabolomics profiling of a breast epithelial cell line and its EMT derived mesenchymal phenotype to create genome-scale metabolic ...
    • Metabolic reprogramming supports the invasive phenotype in malignant melanoma 

      Bettum, Ingrid Johanne; Gorad, Saurabh Sayajirao; Barkovskaya, Anna; Pettersen, Solveig; Moestue, Siver Andreas; Vasiliauskaite, Kotryna; Tenstad, Ellen; Øyjord, Tove Ragnhild; Risa, Øystein; Nygaard, Vigdis; Mælandsmo, Gunhild; Prasmickaite, Lina (Journal article; Tidsskriftartikkel, 2015)
      Invasiveness is a hallmark of aggressive cancer like malignant melanoma, and factors involved in acquisition or maintenance of an invasive phenotype are attractive targets for therapy. We investigated melanoma phenotype modulation induced by the metastasis-promoting microenvironmental protein S100A4, focusing on the relationship between enhanced cellular motility, dedifferentiation and metabolic ...
    • O-GlcNAc Transferase Inhibition Differentially Affects Breast Cancer Subtypes 

      Barkovskaya, Anna; Seip, Kotryna; Hilmarsdòttir, Bylgja; Mælandsmo, Gunhild Mari; Moestue, Siver Andreas; Itkonen, Harri (Journal article; Tidsskriftartikkel; Peer reviewed, 2019-04-05)
      Post-translational modifcation of intracellular proteins with a single N-acetylglucosamine sugar (O-GlcNAcylation) regulates signaling, proliferation, metabolism and protein stability. In breast cancer, expression of the enzyme that catalyzes O-GlcNAcylation – O-GlcNAc-transferase (OGT), and the extent of protein O-GlcNAcylation, are upregulated in tumor tissue, and correlate with cancer progression. ...