Jasmonic Acid Induces Endoplasmic Reticulum Stress with Different Outcome in Cultured Normal and Tumor Epidermal Cells

Plant hormones produce cytotoxic effect on human cells and can trigger the processes unrelated to cell death, e.g., biosynthetic system stress. The goal of this study was to investigate activation of the endoplasmic reticulum (ER) stress by jasmonic acid (JA) and to distinguish between the responses...

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Bibliographic Details
Published in:Biochemistry (Moscow) 2019-09, Vol.84 (9), p.1047-1056
Main Authors: Vildanova, M. S., Saidova, A. A., Fokin, A. I., Potashnikova, D. M., Onishchenko, G. E., Smirnova, E. A.
Format: Article
Language:English
Subjects:
Analysis
Biochemistry
Biomedical and Life Sciences
Biomedicine
Bioorganic Chemistry
Biotechnology
Cell death
Cell differentiation
Cell proliferation
Cytotoxicity
Diagnosis
Endoplasmic reticulum
Eutrophication
Gene expression
Genes
Golgi cells
Hormones
Influence
Jasmonates
Jasmonic acid
Life Sciences
Menopause
Microbiology
Physiological aspects
Plant cells
Plant hormones
Skin tumors
Stress (Physiology)
Transcription activation
Tumor cells
Tumors
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Summary:Plant hormones produce cytotoxic effect on human cells and can trigger the processes unrelated to cell death, e.g., biosynthetic system stress. The goal of this study was to investigate activation of the endoplasmic reticulum (ER) stress by jasmonic acid (JA) and to distinguish between the responses of cultured immortalized non-tumorigenic HaCaT cells and epidermoid carcinoma A431 cells to this plant hormone. JA was used in the concentration of 2 mM, as it suppressed cell proliferation in both cell lines. We analyzed expression of genes associated with the activation of ER stress ( GRP78 , ATF4 , CHOP ), the structure of the ER and Golgi complex, and synthetic processes in the HaCaT and A431 cell lines. JA induced expression of genes responsible for the activation of ER stress and caused hypertrophic changes in the Golgi complex in both cell lines. However, the patterns of gene expression in the HaCaT and A431 cells were different, and higher levels of involucrin synthesis were observed in A431 but not in HaCaT cells, suggesting that JA activated differentiation of the tumor A431 cells only. Therefore, JA induced ER stress in both cell lines, but the consequences of ER stress were different for the epidermal immortalized non-tumorigenic and tumor cells.
ISSN:0006-2979
1608-3040
DOI:10.1134/S0006297919090074