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Effects of 17β-estradiol and estrogen receptor subtype-specific agonists on Jurkat E6.1 T-cell leukemia cells
Rahul S Nair1, Mantavya N Patel2, Thangamani Kannan2
1Inspire Laboratory, Institute of Advanced Research in Health Sciences, Tamil Nadu Government Multi Super Speciality Hospital, Chennai, Tamil Nadu, India; Integrative Medicine Laboratory, Department of Biotechnology, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.
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).
