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Proliferative and anti-proliferative effects of thymosin alpha1 on cells are associated with manipulation of cellular ROS levels.

Abstract
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 (Talpha1) 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 Talpha1. In this study, the Talpha1-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 Talpha1 exhibited lower ROS level and higher GSH level. In addition, after treatment with Talpha1, the population of leukomonocytes in the G(2) phase increased, resulting in a slight increase in viability. However, in Talpha1-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 Talpha1 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 Talpha1 as an antitumor drug.
AuthorsYong Qin, Fu-Ding Chen, Liang Zhou, Xing-Guo Gong, Qi-Feng Han
JournalChemico-biological interactions (Chem Biol Interact) Vol. 180 Issue 3 Pg. 383-8 (Aug 14 2009) ISSN: 1872-7786 [Electronic] Ireland
PMID19442654 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents
  • Reactive Oxygen Species
  • Thymosin
  • Proto-Oncogene Proteins c-akt
  • Glutathione
  • Thymalfasin
Topics
  • Animals
  • Antineoplastic Agents (pharmacology)
  • Cell Line, Tumor
  • Cell Proliferation (drug effects)
  • G1 Phase
  • G2 Phase
  • Glutathione (metabolism)
  • Humans
  • Mice
  • Monocytes (drug effects)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • Reactive Oxygen Species (metabolism)
  • Thymalfasin
  • Thymosin (analogs & derivatives, pharmacology)

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