CFP suppresses breast cancer cell growth by TES-mediated upregulation of the transcription factor DDIT3

Ines Block, Carolin Müller, Daniel Sdogati, Henriette Pedersen, Markus List, Aleksandra M Jaskot, Silje Damkjær Syse, Pernille Lund Hansen, Steffen Schmidt, Helle Christiansen, Cinzia Casella, Sidsel Bering Olsen, Monica M Blomstrøm, Angela Riedel, Mads Thomassen, Torben A Kruse, Søren W Karlskov Hansen, Petra Kioschis, Jan Mollenhauer

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Breast cancer is a heterogeneous genetic disease driven by the accumulation of individual mutations per tumor. Whole-genome sequencing approaches have identified numerous genes with recurrent mutations in primary tumors. Although mutations in well characterized tumor suppressors and oncogenes are overrepresented in these sets, the majority of the genetically altered genes have so far unknown roles in breast cancer progression. To improve the basic understanding of the complex disease breast cancer and to potentially identify novel drug targets or regulators of known cancer-driving pathways, we analyzed 86 wild-type genes and 94 mutated variants for their effect on cell growth using a serially constructed panel of MCF7 cell lines. We demonstrate in subsequent experiments that the metal cation transporter CNNM4 regulates growth by induction of apoptosis and identified a tumor suppressive role of complement factor properdin (CFP) in vitro and in vivo. CFP appears to induce the intracellular upregulation of the pro-apoptotic transcription factor DDIT3 which is associated with endoplasmic reticulum-stress response.

Original languageEnglish
JournalOncogene
Volume38
Issue number23
Pages (from-to)4560-4573
ISSN0950-9232
DOIs
Publication statusPublished - 6. Jun 2019

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