Toxicology in vitro : an international journal published in association with BIBRA · 2025
Effects of 17β-estradiol and estrogen receptor subtype-specific agonists on Jurkat E6.1 T-cell leukemia cells.
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Nair Rahul S, Patel Mantavya N, Kannan Thangamani, Gour Shaili, Hariharan Murali M, Prasanna Vijayarengamani, Thirumalai Anupriya, Chockalingam Ramanathan, Vasantharekha Ramasamy, ThyagaRajan Srinivasan, Priyanka Hannah P
Аннотация
BACKGROUND: Estrogen signaling plays a crucial role in immune regulation and cancer metabolism, yet its impact on T-cell leukemia remains unclear. In hematological malignancies, estrogen receptor (ER) activation may influence metabolic shifts that affect cell survival and proliferation. This study investigates the in vitro effects of 17β-estradiol and estrogen receptor subtype-specific agonists on Jurkat E6.1 T-cell leukemia cells.
PURPOSE: To assess how estrogen signaling influences metabolic reprogramming, inflammatory response, and survival pathways in Jurkat E6.1 cells through receptor-dependent and independent mechanisms.
METHODS: Jurkat E6.1 cells incubated with different concentrations of 17β-estradiol (10-12 M, 10-10 M, 10-8 M) or ER-α agonist 4,4',4″-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (10-10 M, 10-8 M, 10-6 M) or ER-β agonist diarylproprionitrile (10-10 M, 10-8 M, 10-6 M) with and without non-specific antagonist ICI 182,780 (10-6 M). The metabolic enzyme activities of hexokinase, pyruvate kinase, and citrate synthase were measured in cell pellets, while supernatants were analyzed for IL-6 and nitric oxide (NO) production. Additionally, PI3K/Akt pathway activation was assessed by measuring p-Akt/Total Akt expression.
RESULTS: A shift from glycolysis to oxidative phosphorylation was observed on treatment with 17β-estradiol with significant decline in hexokinase activity and a concomitant increase in activities of pyruvate kinase and citrate synthase.
CONCLUSION: 17β-estradiol mediates its effects on Jurkat E6.1 cells in vitro through receptor-subtype dependent and independent mechanisms involving metabolic enzymes (hexokinase, pyruvate kinase, citrate synthase), cytokines (IL-6), nitric oxide, and signaling molecules (p-Akt).
PURPOSE: To assess how estrogen signaling influences metabolic reprogramming, inflammatory response, and survival pathways in Jurkat E6.1 cells through receptor-dependent and independent mechanisms.
METHODS: Jurkat E6.1 cells incubated with different concentrations of 17β-estradiol (10-12 M, 10-10 M, 10-8 M) or ER-α agonist 4,4',4″-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (10-10 M, 10-8 M, 10-6 M) or ER-β agonist diarylproprionitrile (10-10 M, 10-8 M, 10-6 M) with and without non-specific antagonist ICI 182,780 (10-6 M). The metabolic enzyme activities of hexokinase, pyruvate kinase, and citrate synthase were measured in cell pellets, while supernatants were analyzed for IL-6 and nitric oxide (NO) production. Additionally, PI3K/Akt pathway activation was assessed by measuring p-Akt/Total Akt expression.
RESULTS: A shift from glycolysis to oxidative phosphorylation was observed on treatment with 17β-estradiol with significant decline in hexokinase activity and a concomitant increase in activities of pyruvate kinase and citrate synthase.
CONCLUSION: 17β-estradiol mediates its effects on Jurkat E6.1 cells in vitro through receptor-subtype dependent and independent mechanisms involving metabolic enzymes (hexokinase, pyruvate kinase, citrate synthase), cytokines (IL-6), nitric oxide, and signaling molecules (p-Akt).