ArticleClinical & experimental metastasis1999
Growth-associated changes in glutathione content correlate with liver metastatic activity of B16 melanoma cells.
Article in Clinical & experimental metastasis, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Metabolic profiling of human melanoma cell lines with high and low metastatic capacity by 1H-NMR spectroscopy.PloS one · 2026Article
- Intracellular Formation of Synthetic Peptide Nanostructures Causes Mitochondrial Disruption and Cell Death in Tumor Spheroids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pt(IV) Complexes as Anticancer Drugs and Their Relationship with Oxidative Stress.Biomedicines · 2025Review
- Gut microbiota-derived formate exacerbates pulmonary metastasis in cancer.Theranostics · 2025Article
- Recent Advances in the Application of Mitochondria-targeted Fluorescent Probes.Current medicinal chemistry · 2025Review
- Charge-Reversal Nano-Drug Delivery Systems in the Tumor Microenvironment: Mechanisms, Challenges, and Therapeutic Applications.International journal of molecular sciences · 2024Review
- GGT5: a potential immunotherapy response inhibitor in gastric cancer by modulating GSH metabolism and sustaining memory CD8+ T cell infiltration.Cancer immunology, immunotherapy : CII · 2024Article
- The Role of Glutathione in the Management of Cell-Mediated Immune Responses in Individuals with HIV.International journal of molecular sciences · 2024Review
- Glutaredoxin 2 Protein (Grx2) as an Independent Prognostic Factor Associated with the Survival of Colon Adenocarcinoma Patients.International journal of molecular sciences · 2024Article
- Lipids as mediators of cancer progression and metastasis.Nature cancer · 2024Review
- ALKBH5-mediated CHAC1 depletion promotes malignant progression and decreases cisplatin-induced oxidative stress in gastric cancer.Cancer cell international · 2023Article
- Glutathione: Lights and Shadows in Cancer Patients.Biomedicines · 2023Review
- Evaluation of Metabolomics as Diagnostic Targets in Oral Squamous Cell Carcinoma: A Systematic Review.Metabolites · 2023Review
- Role of pyroglutamic acid in cumulus cells of women with polycystic ovary syndrome.Journal of assisted reproduction and genetics · 2022Article
- NAC, NAC, Knockin' on Heaven's door: Interpreting the mechanism of action of N-acetylcysteine in tumor and immune cells.Redox biology · 2022Review
- Article
- Metabolic Adaptation-Mediated Cancer Survival and Progression in Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Fluorinated diselenide nanoparticles for radiosensitizing therapy of cancer.Free radical biology & medicine · 2022Article
- Designing bioresponsive nanomaterials for intracellular self-assembly.Nature reviews. Chemistry · 2022Review
- Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B16 melanoma (B16M) was used to study the relationship between glutathione (GSH) metabolism and the metastatic activity of malignant cells. GSH content increased in B16M cells during the initial period of exponential growth in vitro, to reach a maximum of 37 +/- 3 nmol/10(6) cells 12 h after plating, and then gradually decreased to control values (10 +/- 2 nmol/10(6) cells) when cultures approached confluency. On the contrary, glutathione disulphide (GSSG) levels (0.5 +/- 0.2 nmol/10(6) cells) and the rate of glutathione efflux (GSH + GSSG) (2.5 +/- 0.4 nmol/10(6) cells per h) remained constant as B16M grew. Changes in enzyme activities involved in GSH synthesis or the glutathione redox cycle did not explain shifts in the glutathione status (GSH/GSSG). However, two facts contributed to explain why GSH levels changed within B16M cells: a) high intracellular levels of GSH induced a feed-back inhibition of its own synthesis in B16M cells from cultures with low cellular density (LD cells); b) transport of cyst(e)ine, whose availability is the major rate-limiting step for GSH synthesis, was limited by cell-cell contact in cultures with high cellular density (HD cells). Intrasplenic injection of B16M cells with high GSH content (exponentially-growing cultures) showed higher metastatic activity in the liver than cells with low GSH content (cells at confluency). However, when low GSH-content cells (HD cells) were incubated in the presence of GSH ester, which rapidly enters the cell and delivers free GSH, their metastatic activity significantly increased. Our results demonstrate that changes in GSH content regulate the metastatic behaviour of B16M cells.
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