The effect of ALA-PDT under normoxia and cobalt chloride (CoCl2)-induced hypoxia on adhesion molecules (ICAM-1, VCAM-1) secretion by colorectal cancer cells

Abstract

BackgroundThe most fundamental problem in cancer biology research is to understand the mechanisms of cancer cell resistance to oncological therapies. Literature reports emphasize the important role of adhesion molecules: intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 (ICAM-1 and VCAM-1) in cancer progression and resistance to treatment. Photodynamic therapy (PDT) could become the component of a personalized approach to colorectal cancer, therefore we examined the effects of ALA (δ-aminolevulinic) acid PDT in normoxia and under cobalt chloride (CoCl2)-induced hypoxia on ICAM-1 and VCAM-1 secretion by colorectal cancer cells. MethodsHuman colorectal cancer cells of different malignant potential SW480 and SW620 were used in the experiment. Cell lines were treated ALA, in order to achieve conditions comparable to in vivo hypoxia, CoCl2 was added, then cells were irradiated both in normoxia and in hypoxia-like conditions. Cell viability was assessed using the LDH and MTT assays and apoptosis. ICAM-1 and VCAM-1 concentrations were determined with the Bio – Plex ProTM Assay and System. ResultsThe experiment revealed that ALA PDT under normoxia and CoCl2-induced hypoxia had no significant effect on ICAM-1 and VCAM-1-dependent adhesion of colorectal cancer cells. The secretion of ICAM-1 by SW480 ell line was more pronounced compared to ICAM-1 secretion by SW620 cells. ConclusionDetermination of tumor marker levels and especially adhesion molecules involved in metastatic spread is necessary. Our experiment reveals, that ALA PDT in normoxia and CoCl2-induced hypoxia has no effect on adhesion molecules secretion by colon cancer cells in vitro.