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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Effect of cortisol on K562 leukemia cells

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Author(s):
Fonseca, Marcelo de Oliveira [1] ; da Silva, Newton Soares [1] ; Soares, Cristina Pacheco [1]
Total Authors: 3
Affiliation:
[1] Univ Vale Paraiba, Sao Paulo, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Revista O Mundo da Saúde; v. 43, n. 4, p. 854-861, OCT-DEC 2019.
Web of Science Citations: 0
Abstract

Numerous studies describe effects caused by stress on the development, progression and poor prognosis of various pathologies, such as cancer. In recent decades, researchers have investigated the role of stress-associated hormones and cancer progression. Cortisol is described as a primary stress hormone in the human body. Studies show a positive correlation of elevated cortisol levels and cancer progression. Increased cell proliferation and increased reactive oxygen species that contribute to DNA damage, dysplasia, and neoplasms are the result of prolonged stress where tissue becomes insensitive to cortisol, the primary human stress hormone. This study explores the influence of cortisol, an important hormone involved in stress, on tumor cell development, particularly in human cells of chronic myeloid leukemia (K562). K562 cells were exposed to increasing cortisol (hydrocortisone) concentrations for 24 or 48 hours and cytotoxicity (MIT assay 13-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazio bromide] and cell death processes (fluorescence microscopy) were investigated. Our data show a considerable role of cortisol not only in mitochondrial activity, but also in the processes of proliferation and apoptotic and necrotic death in K562 cells. These results demonstrate the possible influence of stress on tumor development and demonstrate that K562 cells can be adapted to cortisol levels over time. (AU)

FAPESP's process: 16/17984-1 - Evaluation glycans, heat shock proteins and fagocitose after photodynamic treatment.
Grantee:Cristina Pacheco Soares
Support type: Regular Research Grants
FAPESP's process: 09/15206-8 - Cellular mechanism of inactivating tumor by photodynamic therapy
Grantee:Cristina Pacheco Soares
Support type: Regular Research Grants