| Title: |
GDF11 downregulates FOXP3 in T-cell acute lymphoblastic leukemia-derived cells and associates with restraining aggressiveness. |
| Authors: |
SáNCHEZ-RODRíGUEZ, MELISSA; LAZZARINI-LECHUGA, ROBERTO; SOUZA-ARROYO, VERóNICA; BUCIO-ORTIZ, LETICIA; MIRANDA-LABRA, ROXANA U.; GERARDO-RAMíREZ, MONSERRAT; PáEZ-ARENAS, ARACELI; VERGARA-MENDOZA, MOISES; CONCEPCIóN GUTIéRREZ-RUIZ, MARíA; ESCOBEDO-CALVARIO, ALEJANDRO; GOMEZ-QUIROZ, LUIS E. |
| Source: |
Oncology Research; 2025, Vol. 33 Issue 8, p2075-2084, 10p |
| Subject Terms: |
Growth differentiation factors; Transcription factors; Reactive oxygen species; Embryology; Cancer cells |
| Abstract: |
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. [ABSTRACT FROM AUTHOR] |
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| Database: |
Complementary Index |