Summary of Study ST003287

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002039. The data can be accessed directly via it's Project DOI: 10.21228/M8253C This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST003287
Study TitleMetabolic profiling and synergistic therapeutic strategies unveil the cytotoxic potential of selenium-chrysin (SeChry) in NSCLC cells
Study SummaryLung cancer ranks as the predominant cause of cancer-related mortalities on a global scale. Despite progress in therapeutic interventions, encompassing surgical procedures, radiation, chemotherapy, targeted therapies and immunotherapy, the overall prognosis remains unfavorable. Imbalances in redox equilibrium and disrupted redox signaling, common traits in tumors, play crucial roles in malignant progression and treatment resistance. Cancer cells, often characterized by persistent high levels of ROS resulting from genetic, metabolic, and microenvironmental alterations, counterbalance this by enhancing their antioxidant capacity. Cysteine availability emerges as a critical factor in chemoresistance, shaping the survival dynamics of non-small cell lung cancer (NSCLC) cells. Selenium-chrysin (SeChry) was disclosed as a modulator of cysteine intracellular availability. This study comprehensively characterizes the metabolism of SeChry in NSCLC. SeChry treatment induces notable metabolic shifts, particularly in selenocompounds metabolism, impacting crucial pathways such as glycolysis, gluconeogenesis, the tricarboxylic acid (TCA) cycle, and amino acid metabolism. Additionally, SeChry affects the levels of key metabolites such as acetate, lactate, glucose, and amino acids, contributing to disruptions in redox homeostasis and cellular biosynthesis.
Institute
ITQB NOVA
Last NameGonçalves
First NameLuís
AddressAvenida Republica
Emaillgafeira@itqb.unl.pt
Phone214469464
Submit Date2024-06-28
Raw Data AvailableYes
Raw Data File Type(s)fid
Analysis Type DetailNMR
Release Date2024-07-22
Release Version1
Luís Gonçalves Luís Gonçalves
https://dx.doi.org/10.21228/M8253C
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR002039
Project DOI:doi: 10.21228/M8253C
Project Title:Metabolic profiling and synergistic therapeutic strategies unveil the cytotoxic potential of selenium-chrysin (SeChry) in NSCLC cells
Project Summary:Lung cancer ranks as the predominant cause of cancer-related mortalities on a global scale. Despite progress in therapeutic interventions, encompassing surgical procedures, radiation, chemotherapy, targeted therapies and immunotherapy, the overall prognosis remains unfavorable. Imbalances in redox equilibrium and disrupted redox signaling, common traits in tumors, play crucial roles in malignant progression and treatment resistance. Cancer cells, often characterized by persistent high levels of ROS resulting from genetic, metabolic, and microenvironmental alterations, counterbalance this by enhancing their antioxidant capacity. Cysteine availability emerges as a critical factor in chemoresistance, shaping the survival dynamics of non-small cell lung cancer (NSCLC) cells. Selenium-chrysin (SeChry) was disclosed as a modulator of cysteine intracellular availability. This study comprehensively characterizes the metabolism of SeChry in NSCLC. SeChry treatment induces notable metabolic shifts, particularly in selenocompounds metabolism, impacting crucial pathways such as glycolysis, gluconeogenesis, the tricarboxylic acid (TCA) cycle, and amino acid metabolism. Additionally, SeChry affects the levels of key metabolites such as acetate, lactate, glucose, and amino acids, contributing to disruptions in redox homeostasis and cellular biosynthesis.
Institute:ITQB NOVA
Last Name:Gonçalves
First Name:Luís
Address:Avenida Republica, Oeiras, Not USCanada, 2780-157 Oeiras, Portugal
Email:lgafeira@itqb.unl.pt
Phone:214469464

Subject:

Subject ID:SU003407
Subject Type:Cultured cells
Subject Species:Homo sapiens
Taxonomy ID:9606

Factors:

Subject type: Cultured cells; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Sample source Cell Line Condition
SA356301AH_aq_A7_230607Non-small cell lung cancer cells A549 Control
SA356302AH_aq_A8_230607Non-small cell lung cancer cells A549 Control
SA356303AH_aq_A2_230607Non-small cell lung cancer cells A549 SeChry
SA356304AH_aq_A1_230607Non-small cell lung cancer cells A549 SeChry
SA356305AH_aq_A6_230607Non-small cell lung cancer cells A549 SeChry
SA356306AH_aq_A3_230607Non-small cell lung cancer cells A549 SeChry
SA356307AH_aq_A4_230607Non-small cell lung cancer cells A549 SeChry
SA356308AH_aq_A5_230607Non-small cell lung cancer cells A549 SeChry
SA356309AH_aq_H8_230607Non-small cell lung cancer cells H292 Control
SA356310AH_aq_H7_230607Non-small cell lung cancer cells H292 Control
SA356311AH_aq_H3_230607Non-small cell lung cancer cells H292 SeChry
SA356312AH_aq_H5_230607Non-small cell lung cancer cells H292 SeChry
SA356313AH_aq_H6_230607Non-small cell lung cancer cells H292 SeChry
SA356314AH_aq_H2_230607Non-small cell lung cancer cells H292 SeChry
SA356315AH_aq_H1_230607Non-small cell lung cancer cells H292 SeChry
SA356316AH_aq_H4_230607Non-small cell lung cancer cells H292 SeChry
SA356317AH_aq_P7_230607Non-small cell lung cancer cells PC9 Control
SA356318AH_aq_P8_230607Non-small cell lung cancer cells PC9 Control
SA356319AH_aq_P1_230607Non-small cell lung cancer cells PC9 SeChry
SA356320AH_aq_P4_230607Non-small cell lung cancer cells PC9 SeChry
SA356321AH_aq_P5_230607Non-small cell lung cancer cells PC9 SeChry
SA356322AH_aq_P6_230607Non-small cell lung cancer cells PC9 SeChry
Showing results 1 to 22 of 22

Collection:

Collection ID:CO003400
Collection Summary:Cells were plated in 175 cm2 T-Flasks: H292 (1.5 × 107 cells/flask); A549 (2 × 107 cells/flask), and PC-9 (2.5 × 107 cells/flask) and exposed to control conditions or SeChry for 24 h. The cells were cultured in Dulbecco’s Modified Eagle’s Medium 1× (DMEM) (41965-039, Gibco, Life Technologies) supplemented with 10% fetal bovine serum (FBS; S 0615, Merck), 1% Antibiotic-Antimycotic (AA; P06-07300, PAN Biotech) and 50 μg/mL Gentamicin (15750-060, Gibco, Life Technologies). H1975, H522 and H596 were cultured in RPMI 1640 (BE12-167F, Lonza) supplemented with 0.58 g/L of L-glutamine, 1% FBS (S 0615, Merck) and 1% antibiotic-antimycotic (AA) (P06-07300, PAN Biotech). Cells were maintained at 37ºC in a humidified environment with 5% CO2. Cells were cultured until an optical confluence of 75–100% and detachment was performed with 0.05% trypsin-EDTA 1× (25300-054, Invitrogen). Before any in vitro experiment, cells were synchronized under starvation (FBS-free culture medium) overnight.
Sample Type:Non-small cell lung cancer cell lines

Treatment:

Treatment ID:TR003416
Treatment Summary:Cells were kept in control conditions or exposed to SeChry. The concentrations of SeChry for each cell line were chosen according to the previously determined half-maximum effective concentrations (EC50).

Sample Preparation:

Sampleprep ID:SP003414
Sampleprep Summary:Culture media (supernatant) was collected and stored at -80 °C. Cell methanol/chloroform/water extracts were performed to separate the aqueous (methanol/water) and organic (chloroform) phases.

Analysis:

Analysis ID:AN005384
Analysis Type:NMR
Analysis Protocol File:LG_NSCLC_SeChry_protocol.txt
Num Factors:6
Num Metabolites:46
Units:nanomoles

NMR:

NMR ID:NM000286
Analysis ID:AN005384
Instrument Name:Bruker Avance II+ 800 MHz
Instrument Type:FT-NMR
NMR Experiment Type:1D-1H
Spectrometer Frequency:800 MHz
NMR Probe:5 mm TCI cryoprobe
NMR Tube Size:5 mm
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