LACTB exerts tumor suppressor properties in epithelial ovarian cancer through regulation of Slug

0564801 - ÚOCHB 2024 RIV US eng J - Journal Article
Cutano, Valentina - Ferreira Mendes, Jessica Marianne - Escudeiro-Lopes, Sara - Machado, Susana - Vinaixa Forner, Judith - Gonzalez-Morena, Juan Manuel - Převorovský, M. - Zemlianski, V. - Feng, Y. - Králová Viziová, Petra - Hartmanová, Andrea - Malčeková, Beata - Jakoubě, Pavel - Iyer, S. - Kečkéšová, Zuzana
LACTB exerts tumor suppressor properties in epithelial ovarian cancer through regulation of Slug.
Life Science Alliance. Roč. 6, č. 1 (2023), č. článku e202201510. E-ISSN 2575-1077
R&D Projects: GA ČR(CZ) GJ18-24473Y; GA MŠMT(CZ) EF19_074/0016322; GA MŠMT LX22NPO5102; GA MŠMT(CZ) LM2018126; GA MŠMT EF18_046/0015861
Institutional support: RVO:61388963 ; RVO:68378050
Keywords : mesenchymal transition * lipid metabolism * fallopian tube
OECD category: Biochemistry and molecular biology; Biochemistry and molecular biology (UMG-J)
Impact factor: 4.4, year: 2022
Method of publishing: Open access
http://doi.org/10.26508/lsa.202201510

Epithelial-mesenchymal transition (EMT) is a cellular mechanism used by cancer cells to acquire migratory and stemness properties. In this study, we show, through in vitro, in vivo, and 3D culture experiments, that the mitochondrial protein LACTB manifests tumor suppressor properties in ovarian cancer. We show that LACTB is significantly down-regulated in epithelial ovarian cancer cells and clinical tissues. Re-expression of LACTB negatively effects the growth of cancer cells but not of non-tumorigenic cells. Mechanistically, we show that LACTB leads to differentiation of ovarian cancer cells and loss of their stemness properties, which is achieved through the inhibition of the EMT program and the LACTB-dependent down-regulation of Snail2/Slug transcription factor. This study uncovers a novel role of LACTB in ovarian cancer and proposes new ways of counteracting the oncogenic EMT program in this model system.
Permanent Link: https://hdl.handle.net/11104/0336392


Research data: ArrayExpress