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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Veröffentlicht in: | Biochemistry (Moscow) 2019-09, Vol.84 (9), p.1047-1056 |
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creator | Vildanova, M. S. Saidova, A. A. Fokin, A. I. Potashnikova, D. M. Onishchenko, G. E. Smirnova, E. A. |
description | 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. |
doi_str_mv | 10.1134/S0006297919090074 |
format | Article |
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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.</description><identifier>ISSN: 0006-2979</identifier><identifier>EISSN: 1608-3040</identifier><identifier>DOI: 10.1134/S0006297919090074</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>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</subject><ispartof>Biochemistry (Moscow), 2019-09, Vol.84 (9), p.1047-1056</ispartof><rights>Pleiades Publishing, Ltd. 2019</rights><rights>COPYRIGHT 2019 Springer</rights><rights>Biochemistry (Moscow) is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-8bc78ddfcc88d513a5a326113faf7739fbff537fa6d502e4943a8126cb3a1f653</citedby><cites>FETCH-LOGICAL-c416t-8bc78ddfcc88d513a5a326113faf7739fbff537fa6d502e4943a8126cb3a1f653</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0006297919090074$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0006297919090074$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids></links><search><creatorcontrib>Vildanova, M. S.</creatorcontrib><creatorcontrib>Saidova, A. A.</creatorcontrib><creatorcontrib>Fokin, A. I.</creatorcontrib><creatorcontrib>Potashnikova, D. M.</creatorcontrib><creatorcontrib>Onishchenko, G. E.</creatorcontrib><creatorcontrib>Smirnova, E. A.</creatorcontrib><title>Jasmonic Acid Induces Endoplasmic Reticulum Stress with Different Outcome in Cultured Normal and Tumor Epidermal Cells</title><title>Biochemistry (Moscow)</title><addtitle>Biochemistry Moscow</addtitle><description>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.</description><subject>Analysis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bioorganic Chemistry</subject><subject>Biotechnology</subject><subject>Cell death</subject><subject>Cell differentiation</subject><subject>Cell proliferation</subject><subject>Cytotoxicity</subject><subject>Diagnosis</subject><subject>Endoplasmic reticulum</subject><subject>Eutrophication</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Golgi cells</subject><subject>Hormones</subject><subject>Influence</subject><subject>Jasmonates</subject><subject>Jasmonic acid</subject><subject>Life Sciences</subject><subject>Menopause</subject><subject>Microbiology</subject><subject>Physiological aspects</subject><subject>Plant cells</subject><subject>Plant hormones</subject><subject>Skin tumors</subject><subject>Stress (Physiology)</subject><subject>Transcription activation</subject><subject>Tumor cells</subject><subject>Tumors</subject><issn>0006-2979</issn><issn>1608-3040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kV1vFCEUhomxiWvrD_COxBtvpvIxA8zlZl21prGJrdeEhUOlmYEVBpv-e1nXpPErXBDO-7wnL-cg9JKSc0p5_-aaECLYKEc6kpEQ2T9BKyqI6jjpyVO0OsjdQX-Gnpdy156MjHyFvn80ZU4xWLy2weGL6KqFgrfRpf3UpCZ8hiXYOtUZXy8ZSsH3YfmK3wbvIUNc8FVdbJoBh4g3dVpqBoc_pTybCZvo8E2dU8bbfXDws7aBaSpn6MSbqcCLX_cp-vJue7P50F1evb_YrC8721OxdGpnpXLOW6uUGyg3g-FMtA9746Xko995P3DpjXADYdCPPTeKMmF33FAvBn6KXh_77nP6VqEseg7FtgQmQqpFM06ZIlJx0tBXf6B3qebY0mnG1MgZbcN9pG7NBDpEn5Zs7KGpXgvCJBVS8Ead_4Nqx0GbaIrgQ6v_ZqBHg82plAxe73OYTX7QlOjDgvVfC24edvSUxsZbyI-B_2_6AS-MphQ</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Vildanova, M. 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A.</creator><general>Pleiades Publishing</general><general>Springer</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20190901</creationdate><title>Jasmonic Acid Induces Endoplasmic Reticulum Stress with Different Outcome in Cultured Normal and Tumor Epidermal Cells</title><author>Vildanova, M. S. ; Saidova, A. A. ; Fokin, A. I. ; Potashnikova, D. M. ; Onishchenko, G. E. ; Smirnova, E. 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S.</au><au>Saidova, A. A.</au><au>Fokin, A. I.</au><au>Potashnikova, D. M.</au><au>Onishchenko, G. E.</au><au>Smirnova, E. A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Jasmonic Acid Induces Endoplasmic Reticulum Stress with Different Outcome in Cultured Normal and Tumor Epidermal Cells</atitle><jtitle>Biochemistry (Moscow)</jtitle><stitle>Biochemistry Moscow</stitle><date>2019-09-01</date><risdate>2019</risdate><volume>84</volume><issue>9</issue><spage>1047</spage><epage>1056</epage><pages>1047-1056</pages><issn>0006-2979</issn><eissn>1608-3040</eissn><abstract>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.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><doi>10.1134/S0006297919090074</doi><tpages>10</tpages></addata></record> |
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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 |
title | Jasmonic Acid Induces Endoplasmic Reticulum Stress with Different Outcome in Cultured Normal and Tumor Epidermal Cells |
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