Proliferative and anti-proliferative effects of thymosin α1 on cells are associated with manipulation of cellular ROS levels

• Published in: Chemico-biological interactions Vol. 180; no. 3; pp. 383 - 388
• Main Authors: Qin, Yong, Chen, Fu-Ding, Zhou, Liang, Gong, Xing-Guo, Han, Qi-Feng
• Format: Journal Article
• Language: English
• Published: Elsevier Ireland Ltd 14.08.2009
• Subjects: Akt pathway; Cell cycle; ROS; Thymosin α1; Thymosin α1; Akt pathway; ROS; Cell cycle
• ISSN: 0009-2797; 1872-7786
• DOI: 10.1016/j.cbi.2009.05.006

Reactive oxygen species (ROS) are constantly generated and eliminated in the biological system and play important roles in a variety of physiological and pathological processes. Previous studies indicate that modulation of cellular ROS affects cell proliferation. Thymosin alpha 1 (Tα1) is a naturally occurring thymic peptide and has previously been shown to be a potential therapy for some immunodeficiencies, malignancies, and infections. However, few reports have focused on manipulation of cellular ROS level effects of Tα1. In this study, the Tα1-treated leukomonocytes, which were isolated from mice spleens, exhibited a higher ROS level and a lower reduced glutathione (GSH) level; however, HepG2 cells treated with Tα1 exhibited lower ROS level and higher GSH level. In addition, after treatment with Tα1, the population of leukomonocytes in the G 2 phase increased, resulting in a slight increase in viability. However, in Tα1-treated HepG2 cells, the cell cycle was delayed in the G 1 phase, thereby inhibiting tumor cell proliferation; in addition, dephosphorylation of the serine/threonine kinase Akt was detected. In conclusion, we show that Tα1 has potent anti-proliferative activity against malignant human hepatoma cells and proliferative activity against leukomonocytes associated with manipulation of oxidative stress levels which indicates the potential of Tα1 as an antitumor drug.