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GDF11 downregulates FOXP3 in T-cell acute lymphoblastic leukemia-derived cells and associates with restraining
Melissa SáNCHEZ-RODRíGUEZ1,2, Roberto Lazzarini-Lechuga3, VERóNICA Souza-Arroyo1,4
1Área de Medicina Experimental y Traslacional, Departamento de Ciencias de la Salud, DCBS, Universidad Autónoma Metropolitana-Iztapalapa, Mexico City, 09340, Mexico.
Background:
Growth differentiation factor 11 (GDF11), a transforming growth factor-beta superfamily member, is a crucial protein involved in many differentiation processes in embryogenesis and morphogenesis, and it has been extensively characterized due to its capacity to target poorly differentiated cells, including transformed or cancer cells.
Aim:
In the present work, we aimed to describe the effects on migration, proliferation, and metabolism in the T-cell acute lymphoblastic leukemia-derived cell line Jurkat.
Methods:
Based on previous evidence, we analyzed metabolic changes exerted by GDF11 and its relationship with the aggressive phenotype.
Results:
We found a profound impact on mitochondrial metabolism and reactive oxygen species content; these were related to a decrement in the expression of the transcription factor forkhead-box-protein P3 (FOXP3), which is highly involved in aggressiveness in leukemia cells; this was verified by a decrement in invasion capacity exhibited by the Jurkat cells under the GDF11 treatment.
Conclusion:
The results position the GDF11 response as a good alternative in the search for new therapeutic options for these diseases.
Insights
Growth Differentiation Factor 11 (GDF11) impacts T-cell acute lymphoblastic leukemia (Jurkat) cell metabolism and reduces their aggressive traits. This suggests GDF11 as a potential therapeutic option for leukemia.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Growth Differentiation Factor 11 (GDF11) is a TGF-beta superfamily member crucial for differentiation during embryogenesis and morphogenesis.
- GDF11 targets poorly differentiated cells, including cancer cells, making it a subject of extensive research.
- Its role in targeting aggressive cell phenotypes is an area of growing interest.
Purpose of the Study:
- To investigate the effects of GDF11 on migration, proliferation, and metabolism in Jurkat cells, a T-cell acute lymphoblastic leukemia (T-ALL) cell line.
- To analyze metabolic alterations induced by GDF11 and their correlation with the aggressive phenotype of leukemia cells.
Main Methods:
- Analysis of metabolic changes in Jurkat cells treated with GDF11.
- Assessment of the relationship between GDF11-induced metabolic shifts and the aggressive phenotype.
- Evaluation of changes in mitochondrial metabolism, reactive oxygen species (ROS) content, and forkhead-box-protein P3 (FOXP3) expression.
Main Results:
- GDF11 significantly impacted mitochondrial metabolism and reactive oxygen species (ROS) levels in Jurkat cells.
- A decrease in FOXP3 expression, a transcription factor linked to leukemia aggressiveness, was observed.
- GDF11 treatment led to a reduction in the invasive capacity of Jurkat cells.
Conclusions:
- GDF11 treatment profoundly affects leukemia cell metabolism and reduces their aggressive characteristics.
- The observed decrease in FOXP3 expression and invasion capacity highlights GDF11's anti-leukemic potential.
- These findings position GDF11 as a promising candidate for developing novel therapeutic strategies against T-ALL.
