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

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.

journal_name

Oncogene

journal_title

Oncogene

authors

Block I,Müller C,Sdogati D,Pedersen H,List M,Jaskot AM,Syse SD,Lund Hansen P,Schmidt S,Christiansen H,Casella C,Bering Olsen S,Blomstrøm MM,Riedel A,Thomassen M,Kruse TA,Karlskov Hansen SW,Kioschis P,Mollenhauer J

doi

10.1038/s41388-019-0739-0

subject

Has Abstract

pub_date

2019-06-01 00:00:00

pages

4560-4573

issue

23

eissn

0950-9232

issn

1476-5594

pii

10.1038/s41388-019-0739-0

journal_volume

38

pub_type

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