TY - JOUR
AU - Chen, Zhiyi
AU - Inague, Alex
AU - Kaushal, Kamini
AU - Fazeli, Gholamreza
AU - Schilling, Danny
AU - Xavier da Silva, Thamara N
AU - Dos Santos, Ancely Ferreira
AU - Cheytan, Tasneem
AU - Freitas, Florencio Porto
AU - Yildiz, Umut
AU - Viviani, Lucas Gasparello
AU - Lima, Rodrigo Santiago
AU - Pinz, Mikaela Peglow
AU - Medeiros, Isadora
AU - Iijima, Thais Satie
AU - Alegria, Thiago Geronimo Pires
AU - Pereira da Silva, Railmara
AU - Diniz, Larissa Regina
AU - Weinzweig, Simon
AU - Klein-Seetharaman, Judith
AU - Trumpp, Andreas
AU - Mañas, Adriana
AU - Hondal, Robert
AU - Bartenhagen, Christoph
AU - Fischer, Matthias
AU - Shimada, Briana K
AU - Seale, Lucia A
AU - Chillon, Thilo Samson
AU - Fabiano, Marietta
AU - Schomburg, Lutz
AU - Schweizer, Ulrich
AU - Netto, Luis E
AU - Meotti, Flavia C
AU - Dick, Tobias P
AU - Alborzinia, Hamed
AU - Miyamoto, Sayuri
AU - Friedmann Angeli, José Pedro
TI - PRDX6 contributes to selenocysteine metabolism and ferroptosis resistance.
JO - Molecular cell
VL - 84
IS - 23
SN - 1097-2765
CY - New York, NY
PB - Elsevier
M1 - DKFZ-2024-02325
SP - 4645–4659.e9
PY - 2024
N1 - DKFZ-ZMBH Alliance / 84(23), pp. 4645–4659.e9
AB - Selenocysteine (Sec) metabolism is crucial for cellular function and ferroptosis prevention and begins with the uptake of the Sec carrier, selenoprotein P (SELENOP). Following uptake, Sec released from SELENOP is metabolized via selenocysteine lyase (SCLY), producing selenide, a substrate for selenophosphate synthetase 2 (SEPHS2), which provides the essential selenium donor, selenophosphate (H2SePO3-), for the biosynthesis of the Sec-tRNA. Here, we discovered an alternative pathway in Sec metabolism mediated by peroxiredoxin 6 (PRDX6), independent of SCLY. Mechanistically, we demonstrate that PRDX6 can readily react with selenide and interact with SEPHS2, potentially acting as a selenium delivery system. Moreover, we demonstrate the functional significance of this alternative route in human cancer cells, revealing a notable association between elevated expression of PRDX6 and human MYCN-amplified neuroblastoma subtype. Our study sheds light on a previously unrecognized aspect of Sec metabolism and its implications in ferroptosis, offering further possibilities for therapeutic exploitation.
KW - cancer metabolism (Other)
KW - cell death (Other)
KW - ferroptosis (Other)
KW - neuroblastoma (Other)
KW - selenium (Other)
KW - selenocysteine metabolism (Other)
LB - PUB:(DE-HGF)16
C6 - pmid:39547224
DO - DOI:10.1016/j.molcel.2024.10.027
UR - https://inrepo02.dkfz.de/record/294550
ER -