Aldea C. 1, Aldea Alina 1, Busca Antonela 2, Panait Marieta 2, Anghel Rodica 2, Gruia Maria Iuliana 2
1 Clinic Hospital Coltea
2 Institute of Oncology “Prof. dr. Al. Trestioreanu” Bucharest
Abstract
Cancer is a group of diseases characterized by the uncontrollable growth and spread of abnormal cells which can lead to death without timely intervention. Tumor growth and metastasis depend on angiogenesis and lymphangiogenesis triggered by chemical signals from tumor cells in a phase of rapid growth. Accumulating evidence over the past several years from both in vitro and in vivo studies has indicated a role for reactive oxygen species (ROS) as a signaling mediator of angiogenesis and metastasis These species has been shown to mediate the effects through induction of transcription factors and genes involved in angiogenesis and metastasis. However, the role of ROS in modulating tumor cell metastasis and angiogenesis has seemed paradoxical: High ROS levels suppress tumor angiogenesis and metastasis by destroying cancer cells, whereas sub-optimal concentrations assist cancer cells in metastasizing Therefore, the elucidation of the mechanisms underlying the angiogenesis in cancer cells is necessary for the development of agents to be used in combination with/instead of standard chemotherapy. Aim of the study is to identify reactive oxygen species production in hypoxic conditions and their role in angiogenesis signaling process. For this purpose they were used hepatoma cells derived from an experimental tumor, maintained in culture and treated with Avastin, following in the dynamics of treatment and in successive administrations, the ROS production in real time by flow cytometry techniques. RS1 cells treated with different concentrations of avastin (7.5 mg/ml, 100 mg/ml, or 150 mg/ml) produce ROS in different levels, demonstrated by a bright green fluorescence and registered in FL1 channel appeared between the negative and positive controls.