ArticleCell chemical biology2016
GSTP1 Is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity.
Article in Cell chemical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.
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Who cites it
96 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cross-ancestry meta-analysis identifies a GSTP1 variant in the polycyclic aromatic hydrocarbons metabolism-related pathway contributing to colorectal cancer susceptibility.Archives of toxicology · 2026Pooled it
- Mitochondrial dynamics: A promising tool for personalized TNBC management.Genes & diseases · 2026Review
- Unveiling the Role of GlutathioneACS pharmacology & translational science · 2026Review
- Insights into the molecular and genetic role of obesity in breast cancer pathogenesis.Cancer biology & therapy · 2025Review
- A20 restriction of nitric oxide production restores macrophage bioenergetic balance.bioRxiv : the preprint server for biology · 2025Article
- A Glutathione S-Transferase Pi Molecular Glue Tethers Splicing Factors and Remodels Cell Metabolism.Journal of the American Chemical Society · 2025Article
- Metabolomics as a tool for understanding and treating triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- [Multi-omics analysis of the relationship between oxidative stress-related gene and prostate cancer].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025Article
- Multiomics analysis of GSTP1 knockdown pancreatic cancer cells reveals key regulators of redox and metabolic homeostasis.Biology open · 2025Article
- The effect of the combination therapy with chlorophyllin, a glutathione transferase P1-1 inhibitor, and docetaxel on triple-negative breast cancer invasion and metastasis in vivo/in vitro.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Investigation of the inhibitory effects of the telomere-targeted compounds on glutathione S-transferase P1.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- A Mutual Interaction Between GSTP1 and p53 Improves the Drug Resistance and Malignant Biology of Pancreatic Cancer.Cancer science · 2025Article
- Population-level allelic dispersion modeling by maelstRom yields genome-wide maps of allele-specific dysregulation during early carcinogenesis.GigaScience · 2025Article
- Article
- GSTP1 knockdown induces metabolic changes affecting energy production and lipid balance in pancreatic cancer cells.Molecular & cellular oncology · 2025Article
- Multifaceted impact of HIV inhibitor dapivirine on triple negative breast cancer cells reveals potential entities as targets for novel therapy.Scientific reports · 2024Article
- Nanodynamo quantifies subcellular RNA dynamics revealing extensive coupling between steps of the RNA life cycle.Nature communications · 2024Article
- HIV-protease inhibitors potentiate the activity of carfilzomib in triple-negative breast cancer.British journal of cancer · 2024Article
- Article
- Revealing the mechanism of 755-nm long-pulsed alexandrite laser in inhibiting infantile hemangioma endothelial cells through transcriptome sequencing.Lasers in medical science · 2024Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Breast cancers possess fundamentally altered metabolism that fuels their pathogenicity. While many metabolic drivers of breast cancers have been identified, the metabolic pathways that mediate breast cancer malignancy and poor prognosis are less well understood. Here, we used a reactivity-based chemoproteomic platform to profile metabolic enzymes that are enriched in breast cancer cell types linked to poor prognosis, including triple-negative breast cancer (TNBC) cells and breast cancer cells that have undergone an epithelial-mesenchymal transition-like state of heightened malignancy. We identified glutathione S-transferase Pi 1 (GSTP1) as a novel TNBC target that controls cancer pathogenicity by regulating glycolytic and lipid metabolism, energetics, and oncogenic signaling pathways through a protein interaction that activates glyceraldehyde-3-phosphate dehydrogenase activity. We show that genetic or pharmacological inactivation of GSTP1 impairs cell survival and tumorigenesis in TNBC cells. We put forth GSTP1 inhibitors as a novel therapeutic strategy for combatting TNBCs through impairing key cancer metabolism and signaling pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.