Evaluation glycans, heat shock proteins and fagocitose after photodynamic treatment.

• Grant number: 16/17984-1
• Support Opportunities: Regular Research Grants
• Start date: May 01, 2017
• End date: April 30, 2019
• Field of knowledge: Biological Sciences - Biophysics - Radiology and Photobiology
• Principal Investigator: Cristina Pacheco Soares
• Grantee: Cristina Pacheco Soares
• Host Institution: Instituto de Pesquisa e Desenvolvimento (IP&D). Universidade do Vale do Paraíba (UNIVAP). São José dos Campos , SP, Brazil

Abstract

Photodynamic therapy (PDT) is a cancer intervention based on the interaction of a photosensitizing drug and a light source. PDT may cause changes in the expression of various cellular elements, impairing cell adhesion, cytoskeleton integrity in cells subjected to treatment. However the cellular changes brought about by this treatment are unknown. performance evaluation of tumor cells and the immune response the same, it has aroused the interest of the scientific community. Changes in surface glycoproteins and glycolipids are some significant features of the tumor malignancy, and are intimately associated with an adhesion, invasion and metastasis of tumor cells. Furthermore, the presence of certain carbohydrates promotes the recognition and phagocytosis of cells by macrophages, allowing the body to orchestrate a defense system to certain types of pathologies. The heat shock proteins may contribute to the success or failure of the treatment, acting on activation of the caspases or by changing the tumor cell surface, promoting the activation or inhibition of apoptosis or phagocytosis process. The cytoskeletal components are involved in the regulation of cell adhesion to various compounds of the extracellular matrix and in the adhesive interactions during the formation of secondary tumors. This project proposes to evaluate the effect of PDT on glycans, heat shock proteins and phagocytosis in breast carcinoma cells and larynx, continuing studies initiated in the evaluation of the cellular mechanisms of photodynamic therapy in tumor inactivation. In order to understand the involvement of membrane glycoproteins in the process of phagocytosis, proteoglycans in cell adhesion as well as the influence of heat shock proteins HSPA5 (GRP78), HSP70 and HSP90, the resistance processes and cell death, are used as experimental model cell lines MCF7 (breast carcinoma), HEp-2 (laryngeal carcinoma) and J774 (mouse macrophages). The evaluation of glycoproteins and proteoglycans is performed by Western blotting, fluorescence microscopy, to APPRAISAL of heat shock proteins is used the actual PCR team. For assessment of phagocytosis is used to strain J774 (mouse macrophage) co-cultured with tumor cells undergoing PDT.The knowledge of cell changes brought about by PDT allow obtaining tools for enhancement or optimization, as well as the customization of anticancer treatment, since this therapy has a low cost and improved efficiency when early applied in respect of radio or chemotherapy . (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

DE FARIA SOUZA, ROBERTA KELLY; SILVA CARVALHO, ISABEL CHAVES; DA CUNHA MENEZES COSTA, CAROLINA GENUNCIO; DA SILVA, NEWTON SOARES; PACHECO-SOARES, CRISTINA. Alteration of Surface Glycoproteins After Photodynamic Therapy. Photomedicine and Laser Surgery, v. 36, n. 8, p. 452-456, AUG 2018. (16/17984-1, 11/05958-2, 09/15206-8, 11/05404-7)

FONSECA, MARCELO DE OLIVEIRA; DA SILVA, NEWTON SOARES; SOARES, CRISTINA PACHECO. Effect of cortisol on K562 leukemia cells. Revista O Mundo da Saúde, v. 43, n. 4, p. 854-861, OCT-DEC 2019. (16/17984-1, 09/15206-8)

FONSECA, M. O.; GODOI, B. H.; DA SILVA, N. S.; PACHECO-SOARES, C.; BASTOS-FILHO, TF; CALDEIRA, EMD; FRIZERA-NETO, A. Evaluation of the Effect of Hydrocortisone in 2D and 3D HEp-2 Cell Culture. XXVII BRAZILIAN CONGRESS ON BIOMEDICAL ENGINEERING, CBEB 2020, v. N/A, p. 5-pg., 2022-01-01. (16/17984-1)