Dataset on the proteomic response during ferroptosis induction via tamoxifen induced GPX4 KO in mouse embryonic fibroblasts

Alexey M Nesterenko; Dmitry A Korzhenevskii; Vasilisa M Tereshchuk; Olga M Kudryashova; Vsevolod V Belousov; Arina G Shokhina

doi:10.1016/j.dib.2023.109170

Dataset on the proteomic response during ferroptosis induction via tamoxifen induced GPX4 KO in mouse embryonic fibroblasts

Data Brief. 2023 Apr 20:48:109170. doi: 10.1016/j.dib.2023.109170. eCollection 2023 Jun.

Authors

Alexey M Nesterenko^{1

2}, Dmitry A Korzhenevskii¹, Vasilisa M Tereshchuk^{2

3}, Olga M Kudryashova¹, Vsevolod V Belousov^{1

2

3}, Arina G Shokhina^{1

2

3}

Affiliations

¹ Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, Moscow 117997, Russia.
² Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Science, Moscow 117997, Russia.
³ Pirogov Russian National Research Medical University, Moscow 117997, Russia.

Abstract

Ferroptosis is a type of programmed cell death distinct from apoptosis and necroptosis that plays an essential role in pathophysiological conditions such as neurodegenerative diseases and tumorigenesis. Massive lipid oxidation in an iron-dependent manner is a hallmark of ferroptosis.This modality of cell death is also characterized by perturbation of several metabolic pathways, predominantly fatty acid metabolism, thiol metabolism, iron homeostasis and the mevalonate pathway. We aimed to acquire data from different timepoints of ferroptotic death in order to get information about the primary and delayed phases of the ferroptotic response. For this purpose, we used model Pfa1 cells, which are 4-OH-TAM-inducible Gpx4^-/- mouse immortalized fibroblasts [1]. GPX4 is one of the main intracellular ferroptosis regulators and inhibiting it is a classic approach to induce ferroptosis. Measuring protein fold changes at different ferroptotic stages and in nontreated Pfa1 cells could give useful information on the activation of genes involved in ferroptosis and non-genomic protein regulation during ferroptotic progression. Bottom-up proteomic data were acquired from samples obtained 24 and 48 hours after genetic induction of ferroptosis. Chromato-mass spectra were registered in DDA mode and are suitable for further label-free quantification. These data might be a valuable proteome basis for further investigation of ferroptosis and complement other available omics.

Keywords: Cell death; Ferroptosis; Glutathione peroxidase-4; Mouse embryonic fibroblasts; Pfa1; Proteomics.