AN1-type zinc finger protein 3 (ZFAND3) is a transcriptional regulator that drives Glioblastoma invasion

Anne Schuster, Eliane Klein, Virginie Neirinckx, Arnon Møldrup Knudsen, Carina Fabian, Ann-Christin Hau, Monika Dieterle, Anais Oudin, Petr V. Nazarov, Anna Golebiewska, Arnaud Muller, Daniel Perez-Hernandez, Sophie Rodius, Gunnar Dittmar, Rolf Bjerkvig, Christel Herold-Mende, Barbara Klink, Bjarne Winther Kristensen and Simone P. Niclou ()
Additional contact information
Anne Schuster: Luxembourg Institute of Health
Eliane Klein: Luxembourg Institute of Health
Virginie Neirinckx: Luxembourg Institute of Health
Arnon Møldrup Knudsen: Odense University Hospital
Carina Fabian: Luxembourg Institute of Health
Ann-Christin Hau: Luxembourg Institute of Health
Monika Dieterle: Luxembourg Institute of Health
Anais Oudin: Luxembourg Institute of Health
Petr V. Nazarov: Luxembourg Institute of Health
Anna Golebiewska: Luxembourg Institute of Health
Arnaud Muller: Luxembourg Institute of Health
Daniel Perez-Hernandez: Luxembourg Institute of Health
Sophie Rodius: Luxembourg Institute of Health
Gunnar Dittmar: Luxembourg Institute of Health
Rolf Bjerkvig: Luxembourg Institute of Health
Christel Herold-Mende: University of Heidelberg
Barbara Klink: Laboratoire National de Santé
Bjarne Winther Kristensen: Odense University Hospital
Simone P. Niclou: Luxembourg Institute of Health

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract The infiltrative nature of Glioblastoma (GBM), the most aggressive primary brain tumor, critically prevents complete surgical resection and masks tumor cells behind the blood brain barrier reducing the efficacy of systemic treatment. Here, we use a genome-wide interference screen to determine invasion-essential genes and identify the AN1/A20 zinc finger domain containing protein 3 (ZFAND3) as a crucial driver of GBM invasion. Using patient-derived cellular models, we show that loss of ZFAND3 hampers the invasive capacity of GBM, whereas ZFAND3 overexpression increases motility in cells that were initially not invasive. At the mechanistic level, we find that ZFAND3 activity requires nuclear localization and integral zinc-finger domains. Our findings indicate that ZFAND3 acts within a nuclear protein complex to activate gene transcription and regulates the promoter of invasion-related genes such as COL6A2, FN1, and NRCAM. Further investigation in ZFAND3 function in GBM and other invasive cancers is warranted.

Date: 2020
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DOI: 10.1038/s41467-020-20029-y

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