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Bisphenol A triggers the malignancy of acute myeloid leukemia cells via regulation of IL‐4 and IL‐6
Acute myeloid leukemia (AML) is a cancer of hematopoietic stem cells with a rapid progression. The progression of AML can be regulated by estrogenic signals. Our present data showed that an industrial endocrine‐disrupting chemical, bisphenol A (BPA), can promote the proliferation of AML cells and de...
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| Published in: | Journal of biochemical and molecular toxicology 2020-01, Vol.34 (1), p.e22412-n/a |
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| creator | Zhang, Suwei Li, Jiazhen Fan, Jingru Wu, Xianheng |
| description | Acute myeloid leukemia (AML) is a cancer of hematopoietic stem cells with a rapid progression. The progression of AML can be regulated by estrogenic signals. Our present data showed that an industrial endocrine‐disrupting chemical, bisphenol A (BPA), can promote the proliferation of AML cells and decrease their sensitivity to daunorubicin and cytarabine treatment. Among the tested cytokines, BPA treatment can decrease the expression of interleukin‐4 (IL‐4) while increasing the expression of IL‐6. Overexpression of IL‐4 or neutralization antibody of IL‐6 (anti‐IL‐6) can attenuate BPA‐induced proliferation of AML cells and reverse BPA‐suppressed chemosensitivity. Furthermore, activation of nuclear factor kappa B is essential for BPA‐induced upregulation of IL‐6 in AML cells. As to IL‐4, BPA can increase the expression of NFAT1 to inhibit its transcription. Collectively, our data showed that BPA can trigger the malignancy of AML cells via regulation of IL‐4 and IL‐6. |
| doi_str_mv | 10.1002/jbt.22412 |
| format | article |
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The progression of AML can be regulated by estrogenic signals. Our present data showed that an industrial endocrine‐disrupting chemical, bisphenol A (BPA), can promote the proliferation of AML cells and decrease their sensitivity to daunorubicin and cytarabine treatment. Among the tested cytokines, BPA treatment can decrease the expression of interleukin‐4 (IL‐4) while increasing the expression of IL‐6. Overexpression of IL‐4 or neutralization antibody of IL‐6 (anti‐IL‐6) can attenuate BPA‐induced proliferation of AML cells and reverse BPA‐suppressed chemosensitivity. Furthermore, activation of nuclear factor kappa B is essential for BPA‐induced upregulation of IL‐6 in AML cells. As to IL‐4, BPA can increase the expression of NFAT1 to inhibit its transcription. Collectively, our data showed that BPA can trigger the malignancy of AML cells via regulation of IL‐4 and IL‐6.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.22412</identifier><identifier>PMID: 31714645</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Acute myeloid leukemia ; AML ; Antibodies ; Antibodies, Neutralizing - immunology ; Benzhydryl Compounds - pharmacology ; Bisphenol A ; BPA ; Cell proliferation ; Cell Proliferation - drug effects ; Cytarabine ; Cytokines ; Daunorubicin ; Disruption ; Estrogens, Non-Steroidal - pharmacology ; Hematopoietic stem cells ; HL-60 Cells ; Humans ; IL‐4 ; IL‐6 ; Interleukin-4 - immunology ; Interleukin-4 - metabolism ; Interleukin-6 - immunology ; Interleukin-6 - metabolism ; Interleukins ; Leukemia ; Leukemia, Myeloid, Acute - metabolism ; Leukemia, Myeloid, Acute - pathology ; Malignancy ; Myeloid leukemia ; Neutralization ; NF-AT1 protein ; NFATC Transcription Factors - metabolism ; Organic chemistry ; Phenols ; Phenols - pharmacology ; proliferation ; Stem cells ; Transcription ; U937 Cells ; Xenoestrogens</subject><ispartof>Journal of biochemical and molecular toxicology, 2020-01, Vol.34 (1), p.e22412-n/a</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3532-62b785e9e6293581d0343a89c7b7e68f8ae191affba7859ca574af601140e603</citedby><cites>FETCH-LOGICAL-c3532-62b785e9e6293581d0343a89c7b7e68f8ae191affba7859ca574af601140e603</cites><orcidid>0000-0001-8407-7520</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31714645$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Suwei</creatorcontrib><creatorcontrib>Li, Jiazhen</creatorcontrib><creatorcontrib>Fan, Jingru</creatorcontrib><creatorcontrib>Wu, Xianheng</creatorcontrib><title>Bisphenol A triggers the malignancy of acute myeloid leukemia cells via regulation of IL‐4 and IL‐6</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>Acute myeloid leukemia (AML) is a cancer of hematopoietic stem cells with a rapid progression. The progression of AML can be regulated by estrogenic signals. Our present data showed that an industrial endocrine‐disrupting chemical, bisphenol A (BPA), can promote the proliferation of AML cells and decrease their sensitivity to daunorubicin and cytarabine treatment. Among the tested cytokines, BPA treatment can decrease the expression of interleukin‐4 (IL‐4) while increasing the expression of IL‐6. Overexpression of IL‐4 or neutralization antibody of IL‐6 (anti‐IL‐6) can attenuate BPA‐induced proliferation of AML cells and reverse BPA‐suppressed chemosensitivity. Furthermore, activation of nuclear factor kappa B is essential for BPA‐induced upregulation of IL‐6 in AML cells. As to IL‐4, BPA can increase the expression of NFAT1 to inhibit its transcription. Collectively, our data showed that BPA can trigger the malignancy of AML cells via regulation of IL‐4 and IL‐6.</description><subject>Acute myeloid leukemia</subject><subject>AML</subject><subject>Antibodies</subject><subject>Antibodies, Neutralizing - immunology</subject><subject>Benzhydryl Compounds - pharmacology</subject><subject>Bisphenol A</subject><subject>BPA</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cytarabine</subject><subject>Cytokines</subject><subject>Daunorubicin</subject><subject>Disruption</subject><subject>Estrogens, Non-Steroidal - pharmacology</subject><subject>Hematopoietic stem cells</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>IL‐4</subject><subject>IL‐6</subject><subject>Interleukin-4 - immunology</subject><subject>Interleukin-4 - metabolism</subject><subject>Interleukin-6 - immunology</subject><subject>Interleukin-6 - metabolism</subject><subject>Interleukins</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - metabolism</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Malignancy</subject><subject>Myeloid leukemia</subject><subject>Neutralization</subject><subject>NF-AT1 protein</subject><subject>NFATC Transcription Factors - metabolism</subject><subject>Organic chemistry</subject><subject>Phenols</subject><subject>Phenols - pharmacology</subject><subject>proliferation</subject><subject>Stem cells</subject><subject>Transcription</subject><subject>U937 Cells</subject><subject>Xenoestrogens</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp10LtOwzAYBWALgbgUBl4AWWKBIdSX2ElGWnEpqsTSPXLSP6mLkxQ7AXXjEXhGngS3KQxITD6yPh39OgidU3JDCWHDZdbeMBZStoeOKUmSgISS7m-zCKSMyBE6cW5JCBFJJA7REacRDWUojlE50m61gLox-Ba3VpclWIfbBeBKGV3Wqs7XuCmwyrvW_63BNHqODXQvUGmFczDG4TefLJSdUa1u6g2fTL8-PkOs6nkf5Sk6KJRxcLZ7B2h2fzcbPwbT54fJ-HYa5FxwFkiWRbGABCRLuIjpnPCQqzjJoywCGRexAppQVRSZ8i7JlYhCVUhCaUhAEj5AV33tyjavHbg2rbTbHKlqaDqXMu4h51IITy__0GXT2dof5xVnhMfC3zBA173KbeOchSJdWV0pu04pSTfjp378dDu-txe7xi6rYP4rf9b2YNiDd21g_X9T-jSa9ZXffi2Nkg</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Zhang, Suwei</creator><creator>Li, Jiazhen</creator><creator>Fan, Jingru</creator><creator>Wu, Xianheng</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8407-7520</orcidid></search><sort><creationdate>202001</creationdate><title>Bisphenol A triggers the malignancy of acute myeloid leukemia cells via regulation of IL‐4 and IL‐6</title><author>Zhang, Suwei ; Li, Jiazhen ; Fan, Jingru ; Wu, Xianheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3532-62b785e9e6293581d0343a89c7b7e68f8ae191affba7859ca574af601140e603</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acute myeloid leukemia</topic><topic>AML</topic><topic>Antibodies</topic><topic>Antibodies, Neutralizing - immunology</topic><topic>Benzhydryl Compounds - pharmacology</topic><topic>Bisphenol A</topic><topic>BPA</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cytarabine</topic><topic>Cytokines</topic><topic>Daunorubicin</topic><topic>Disruption</topic><topic>Estrogens, Non-Steroidal - pharmacology</topic><topic>Hematopoietic stem cells</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>IL‐4</topic><topic>IL‐6</topic><topic>Interleukin-4 - immunology</topic><topic>Interleukin-4 - metabolism</topic><topic>Interleukin-6 - immunology</topic><topic>Interleukin-6 - metabolism</topic><topic>Interleukins</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Acute - metabolism</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Malignancy</topic><topic>Myeloid leukemia</topic><topic>Neutralization</topic><topic>NF-AT1 protein</topic><topic>NFATC Transcription Factors - metabolism</topic><topic>Organic chemistry</topic><topic>Phenols</topic><topic>Phenols - pharmacology</topic><topic>proliferation</topic><topic>Stem cells</topic><topic>Transcription</topic><topic>U937 Cells</topic><topic>Xenoestrogens</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Suwei</creatorcontrib><creatorcontrib>Li, Jiazhen</creatorcontrib><creatorcontrib>Fan, Jingru</creatorcontrib><creatorcontrib>Wu, Xianheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Suwei</au><au>Li, Jiazhen</au><au>Fan, Jingru</au><au>Wu, Xianheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bisphenol A triggers the malignancy of acute myeloid leukemia cells via regulation of IL‐4 and IL‐6</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2020-01</date><risdate>2020</risdate><volume>34</volume><issue>1</issue><spage>e22412</spage><epage>n/a</epage><pages>e22412-n/a</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>Acute myeloid leukemia (AML) is a cancer of hematopoietic stem cells with a rapid progression. The progression of AML can be regulated by estrogenic signals. Our present data showed that an industrial endocrine‐disrupting chemical, bisphenol A (BPA), can promote the proliferation of AML cells and decrease their sensitivity to daunorubicin and cytarabine treatment. Among the tested cytokines, BPA treatment can decrease the expression of interleukin‐4 (IL‐4) while increasing the expression of IL‐6. Overexpression of IL‐4 or neutralization antibody of IL‐6 (anti‐IL‐6) can attenuate BPA‐induced proliferation of AML cells and reverse BPA‐suppressed chemosensitivity. Furthermore, activation of nuclear factor kappa B is essential for BPA‐induced upregulation of IL‐6 in AML cells. As to IL‐4, BPA can increase the expression of NFAT1 to inhibit its transcription. Collectively, our data showed that BPA can trigger the malignancy of AML cells via regulation of IL‐4 and IL‐6.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31714645</pmid><doi>10.1002/jbt.22412</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-8407-7520</orcidid></addata></record> |
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| subjects | Acute myeloid leukemia AML Antibodies Antibodies, Neutralizing - immunology Benzhydryl Compounds - pharmacology Bisphenol A BPA Cell proliferation Cell Proliferation - drug effects Cytarabine Cytokines Daunorubicin Disruption Estrogens, Non-Steroidal - pharmacology Hematopoietic stem cells HL-60 Cells Humans IL‐4 IL‐6 Interleukin-4 - immunology Interleukin-4 - metabolism Interleukin-6 - immunology Interleukin-6 - metabolism Interleukins Leukemia Leukemia, Myeloid, Acute - metabolism Leukemia, Myeloid, Acute - pathology Malignancy Myeloid leukemia Neutralization NF-AT1 protein NFATC Transcription Factors - metabolism Organic chemistry Phenols Phenols - pharmacology proliferation Stem cells Transcription U937 Cells Xenoestrogens |
| title | Bisphenol A triggers the malignancy of acute myeloid leukemia cells via regulation of IL‐4 and IL‐6 |
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