Abstract
Photodynamic therapy with hypericin (HY-PDT) and hyperforin (HP) could be treatment modalities for colorectal cancer (CRC), but evidence of their effect on angiogenic factors in CRC is missing. Convenient experimental model utilization is essential for angiogenesis research. Therefore, not only 2D cell models, but also 3D cell models and micro-tumors were used and compared. The micro-tumor extent and interconnection with the chorioallantoic membrane (CAM) was determined by histological analyses. The presence of proliferating cells and HY penetration into the tumor mass were detected by fluorescence microscopy. The metabolic activity status was assessed by an colorimetric assay for assessing cell metabolic activity (MTT assay) and HY accumulation was determined by flow cytometry. Pro-angiogenic factor expression was determined by Western blot and quantitative real-time polymerase chain reaction (RT-qPCR). We confirmed the cytotoxic effect of HY-PDT and HP and showed that their effect is influenced by structural characteristics of the experimental model. We have pioneered a method for analyzing the effect of HP and cellular targeted HY-PDT on pro-angiogenic factor expression in CRC micro-tumors. Despite the inhibitory effect of HY-PDT and HP on CRC, the increased expression of some pro-angiogenic factors was observed. We also showed that CRC experimental micro-tumors created on quail CAM could be utilized for analyses of gene and protein expression.
Highlights
In 1971, Judah Folkman stated the hypothesis that solid tumors are angiogenesis-dependent [1]
A key effort is currently focused on the validation of biomarkers with potential anti-angiogenic effects in order to improve the cure for colorectal cancer (CRC)
The results from clinical studies show that the presence of some angiogenic factors, like vascular endothelial growth factor A (VEGF-A), platelet-derived endothelial cell growth factor (PD-ECGF), and fibroblast growth factor 2 (FGF-2), in serum or tumor tissue is associated with the development of the disease in CRC patients
Summary
In 1971, Judah Folkman stated the hypothesis that solid tumors are angiogenesis-dependent [1]. The majority of human tumors persist in situ for months or years without neovascularization and their size is limited to a small volume of a few cubic millimeters. The beginning of their development is associated with the switch to the angiogenic phenotype, which is linked to the recruitment of new blood vessels that support the growth of both angiogenic and non-angiogenic tumor cells [3]. There is huge evidence of agents with antiangiogenic potential as chemotherapeutics and multikinase and topoisomerase inhibitors for CRC treatment approved mainly in combination with bevacizumab (reviewed in [5]). The results from clinical studies show that the presence of some angiogenic factors, like vascular endothelial growth factor A (VEGF-A), platelet-derived endothelial cell growth factor (PD-ECGF), and fibroblast growth factor 2 (FGF-2), in serum or tumor tissue is associated with the development of the disease in CRC patients (reviewed in [6,7])
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