Comparison Log
2024-12-01 06:47:51.298717
mwtab Python Library Version: 1.2.5
Source:      https://www.metabolomicsworkbench.org/rest/study/analysis_id/AN005353/mwtab/...
Study ID:    ST003267
Analysis ID: AN005353
Status:      Inconsistent

Sections "STUDY" contain missmatched items: {('SUBMIT_DATE', '2023-10-16'), ('STUDY_SUMMARY', 'Recent studies report molecular mechanisms underlying iron-sulfur cluster (Fe-S) biosynthesis and suggest its importance in health and disease. However, a role for Fe-S biosynthesis in cancer contexts remains unclear. Here we report that FDX2, an Fe-S assembly factor, is indispensable for maintenance of cellular Fe-S-containing proteins (Fe-S protein(s)) and proliferation of ovarian cancer (OVC) cells. CRISPR-screening of all metabolism-related genes in OVC cells identified several Fe-S assembly genes as essential for OVC growth. Using an inducible FDX2-KO OVC line, we found that FDX2 loss promotes either senescence-like growth arrest or cell death, depending on TP53 status. Mechanistically, FDX2-loss caused global but differential post transcriptional down-regulation of Fe-S proteins, in turn perturbing respiration, iron-regulation and redox homeostasis, all associated with DNA damage. These results demonstrate significant roles for Fe-S biosynthesis in OVC proliferation and survival and provide information about how the cellular Fe-S-protein network responds to disruptions in Fe-S assembly.'), ('STUDY_SUMMARY', 'Recent studies report molecular mechanisms underlying iron-sulfur cluster (Fe-S) biosynthesis and suggest its importance in health and disease. However, a role for Fe-S biosynthesis in cancer contexts remains unclear. Here we report that FDX2, an Fe-S assembly factor, is indispensable for maintenance of cellular Fe-S-containing proteins (Fe-S protein(s)) and proliferation of ovarian cancer (OVC) cells. CRISPR-screening of all metabolism-related genes in OVC cells identified several Fe-S assembly genes as essential for OVC growth. Using an inducible FDX2-KO OVC line, we found that FDX2 loss promotes either senescence-like growth arrest or cell death, depending on p53 status. Mechanistically, FDX2-loss caused global but differential post transcriptional down-regulation of Fe-S proteins, in turn perturbing respiration, iron-regulation and redox homeostasis, all associated with DNA damage. These results demonstrate significant roles for Fe-S biosynthesis in OVC proliferation and survival and provide information about how the cellular Fe-S-protein network responds to disruptions in Fe-S assembly.')}
Sections "PROJECT" contain missmatched items: {('PUBLICATIONS', 'https://doi.org/10.1016/j.jbc.2024.107678, https://www.jbc.org/article/S0021-9258(24)02179-3/fulltext, https://pubmed.ncbi.nlm.nih.gov/39151727/'), ('DOI', 'http://dx.doi.org/10.21228/M8BJ9X'), ('PROJECT_SUMMARY', 'Recent studies report molecular mechanisms underlying iron-sulfur cluster (Fe-S) biosynthesis and suggest its importance in health and disease. However, a role for Fe-S biosynthesis in cancer contexts remains unclear. Here we report that FDX2, an Fe-S assembly factor, is indispensable for maintenance of cellular Fe-S-containing proteins (Fe-S protein(s)) and proliferation of ovarian cancer (OVC) cells. CRISPR-screening of all metabolism-related genes in OVC cells identified several Fe-S assembly genes as essential for OVC growth. Using an inducible FDX2-KO OVC line, we found that FDX2 loss promotes either senescence-like growth arrest or cell death, depending on TP53 status. Mechanistically, FDX2-loss caused global but differential post transcriptional down-regulation of Fe-S proteins, in turn perturbing respiration, iron-regulation and redox homeostasis, all associated with DNA damage. These results demonstrate significant roles for Fe-S biosynthesis in OVC proliferation and survival and provide information about how the cellular Fe-S-protein network responds to disruptions in Fe-S assembly.'), ('PROJECT_SUMMARY', 'Recent studies report molecular mechanisms underlying iron-sulfur cluster (Fe-S) biosynthesis and suggest its importance in health and disease. However, a role for Fe-S biosynthesis in cancer contexts remains unclear. Here we report that FDX2, an Fe-S assembly factor, is indispensable for maintenance of cellular Fe-S-containing proteins (Fe-S protein(s)) and proliferation of ovarian cancer (OVC) cells. CRISPR-screening of all metabolism-related genes in OVC cells identified several Fe-S assembly genes as essential for OVC growth. Using an inducible FDX2-KO OVC line, we found that FDX2 loss promotes either senescence-like growth arrest or cell death, depending on p53 status. Mechanistically, FDX2-loss caused global but differential post transcriptional down-regulation of Fe-S proteins, in turn perturbing respiration, iron-regulation and redox homeostasis, all associated with DNA damage. These results demonstrate significant roles for Fe-S biosynthesis in OVC proliferation and survival and provide information about how the cellular Fe-S-protein network responds to disruptions in Fe-S assembly.')}
Sections "TREATMENT" contain missmatched items: {('TREATMENT_SUMMARY', 'FDX2-iKO JHOC5 cells were cultured 5 days with or without doxycycline (30 ng/ml) and collected.'), ('TREATMENT_SUMMARY', 'FDX2-iKO JHOC5 cells were cultured 5 days with or without doxycycline (30 ng/ml) and collected. Metabolome data were normalized to protein amounts of cells (shown in "Study design") used for the metabolite extraction.')}
'Metabolites' section of 'MS_METABOLITE_DATA' block do not match.
'Data' section of 'MS_METABOLITE_DATA' block do not match.