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Search: onr:"swepub:oai:DiVA.org:uu-494832" > Targeting SOX2 in g...

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Targeting SOX2 in glioblastoma cells reveals heterogeneity in SOX2 dependency

Dalmo, Erika (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi,Bengt Westermark
Rosén, Gabriela (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi,Fredrik Swartling
Niklasson, Mia (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi,Bengt Westermark
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Bergström, Tobias, 1980- (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi
Miletic, Hrvoje (author)
University of Bergen, Department of Biomedicine; Haukeland University Hospital, Department of Pathology
Lindskog, Cecilia (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi
Forsberg Nilsson, Karin, 1963- (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi
Nelander, Sven (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi
Uhrbom, Lene (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi
Swartling, Fredrik J., 1975- (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi
Westermark, Bengt (author)
Uppsala universitet,Institutionen för immunologi, genetik och patologi
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English.
  • Other publication (other academic/artistic)
Abstract Subject headings
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  • Glioblastoma (GBM) is a lethal disease with no curative treatment. SOX2 is a stem cell transcription factor which is widely expressed across human GBM tumors. Downregulation of SOX2 inhibits tumor formation and its depletion leads to a complete stop of cell proliferation. Despite its known important role in GBM, there is a lack of SOX2 overexpression studies in human GBM cells cultured under stem cell conditions. Previous work in our lab suggests that SOX2 levels need to be precisely maintained for GBM cells to thrive. In this project, we have investigated how altered SOX2 expression affects primary human GBM lines. We found that elevated SOX2 expression inhibited proliferation in a dose-dependent manner in three out of four GBM cell lines. Global gene expression in the resistant line was shifted towards that of the proliferation-inhibited lines upon SOX2 induction. However, SOX2 induction also led to an increase in a GBM stem cell injury response phenotype, which was not present in proliferation-inhibited lines. Furthermore, CRISPR/Cas9-mediated SOX2 knockout revealed a SOX2 independence in the resistant cell line, where SOX2-negative cells could be propagated both in vitro and in vivo.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cancer and Oncology (hsv//eng)

Keyword

Glioblastoma
SOX2

Publication and Content Type

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