Foxo3a expression and acetylation regulate cancer cell growth and sensitivity to cisplatin
Many advanced cancers receive cisplatin‐based chemotherapy. However, cisplatin resistance is a major obstacle for cancer chemotherapy. Foxo3a is a member of the Foxo transcription factor family, which modulates the expression of genes involved in DNA damage repair, apoptosis, and other cellular proc...
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| Veröffentlicht in: | Cancer science 2010-05, Vol.101 (5), p.1177-1185 |
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| creator | Shiota, Masaki Yokomizo, Akira Kashiwagi, Eiji Tada, Yasuhiro Inokuchi, Junichi Tatsugami, Katsunori Kuroiwa, Kentaro Uchiumi, Takeshi Seki, Narihito Naito, Seiji |
| description | Many advanced cancers receive cisplatin‐based chemotherapy. However, cisplatin resistance is a major obstacle for cancer chemotherapy. Foxo3a is a member of the Foxo transcription factor family, which modulates the expression of genes involved in DNA damage repair, apoptosis, and other cellular processes. In this study, we found that cisplatin‐resistant cells were more sensitive to the anticancer agent mithramycin than their parental cells, and had a decreased level of Foxo3a expression. Foxo3a knockdown increased cell proliferation and resistance to cisplatin. On the other hand, mithramycin stimulated Foxo3a expression through reactive oxygen species production and sensitized cells to cisplatin, which was abolished by Foxo3a knockdown, while the acetylation status of Foxo3a was decreased in response to cisplatin treatment and was lower in cisplatin‐resistant cells. Knockdown of Foxo3a‐associated acetyltransferase p300 promoted cancer‐cell growth and cisplatin resistance. In addition, non‐acetylation‐mimicking Foxo3a overexpression decreased cancer cell growth and sensitized cells to cisplatin less than wild‐type Foxo3a overexpression. The current work may contribute to the evaluation of the therapeutic potential of inducing the Foxo3a pathway and acetylating the Foxo3a transcription factor, and lead to the reevaluation of cancer treatments based on mithramycin.
(Cancer Sci 2010; 101: 1177–1185) |
| doi_str_mv | 10.1111/j.1349-7006.2010.01503.x |
| format | Article |
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(Cancer Sci 2010; 101: 1177–1185)</description><subject>Acetylation</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cisplatin - pharmacology</subject><subject>Drug Resistance, Neoplasm</subject><subject>Forkhead Box Protein O3</subject><subject>Forkhead Transcription Factors - analysis</subject><subject>Forkhead Transcription Factors - physiology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Original</subject><subject>Plicamycin - pharmacology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcFuEzEQhi0EoqXwCsgXxGnD2F571weEqogCUiUOLRcultc7mzrarIO9aZO3x5uE0J7AF4893z-e8U8IZTBjeX1YzpgodVEBqBmHfAtMgphtn5HzU-L5Pq4KDYKfkVcpLQGEKnX5kpxx4Awqrc7Jz6uwDcJS3K4jpuTDQO3QUutw3PV2nM4RF5scInV2cBipw76nixgexrs9m3BIfvT3ftzRMVDn03pSDq_Ji872Cd8c9wvy4-rz7fxrcf39y7f55XXhlJSiwKbSWjbQCUTLwdVCtnXHqrrJU7Rd20mrmWqcgpKXAp1seFUrZ0uhWnCuEhfk06HuetOssHU4jNH2Zh39ysadCdabp5nB35lFuDf5J6UuYarw_lghhl8bTKNZ-TSNaQcMm2SqUgkQWsG_SSG41FrXmawPpIshpYjdqSEG08vMLM3klZm8MpOJZm-i2Wbp28cDnYR_XMvAuyNgk7N9F7MxPv3leA2V4jxzHw_cg-9x998NmPnlzRSJ3w60ubk</recordid><startdate>201005</startdate><enddate>201005</enddate><creator>Shiota, Masaki</creator><creator>Yokomizo, Akira</creator><creator>Kashiwagi, Eiji</creator><creator>Tada, Yasuhiro</creator><creator>Inokuchi, Junichi</creator><creator>Tatsugami, Katsunori</creator><creator>Kuroiwa, Kentaro</creator><creator>Uchiumi, Takeshi</creator><creator>Seki, Narihito</creator><creator>Naito, Seiji</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><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>7X8</scope><scope>7TM</scope><scope>5PM</scope></search><sort><creationdate>201005</creationdate><title>Foxo3a expression and acetylation regulate cancer cell growth and sensitivity to cisplatin</title><author>Shiota, Masaki ; Yokomizo, Akira ; Kashiwagi, Eiji ; Tada, Yasuhiro ; Inokuchi, Junichi ; Tatsugami, Katsunori ; Kuroiwa, Kentaro ; Uchiumi, Takeshi ; Seki, Narihito ; Naito, Seiji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6553-eb7995b0f3eea20c835d8f178b700dfdf5a916bc604243ec5b2786ca436d0cc73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acetylation</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cisplatin - pharmacology</topic><topic>Drug Resistance, Neoplasm</topic><topic>Forkhead Box Protein O3</topic><topic>Forkhead Transcription Factors - analysis</topic><topic>Forkhead Transcription Factors - physiology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Original</topic><topic>Plicamycin - pharmacology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shiota, Masaki</creatorcontrib><creatorcontrib>Yokomizo, Akira</creatorcontrib><creatorcontrib>Kashiwagi, Eiji</creatorcontrib><creatorcontrib>Tada, Yasuhiro</creatorcontrib><creatorcontrib>Inokuchi, Junichi</creatorcontrib><creatorcontrib>Tatsugami, Katsunori</creatorcontrib><creatorcontrib>Kuroiwa, Kentaro</creatorcontrib><creatorcontrib>Uchiumi, Takeshi</creatorcontrib><creatorcontrib>Seki, Narihito</creatorcontrib><creatorcontrib>Naito, Seiji</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Nucleic Acids Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Shiota, Masaki</au><au>Yokomizo, Akira</au><au>Kashiwagi, Eiji</au><au>Tada, Yasuhiro</au><au>Inokuchi, Junichi</au><au>Tatsugami, Katsunori</au><au>Kuroiwa, Kentaro</au><au>Uchiumi, Takeshi</au><au>Seki, Narihito</au><au>Naito, Seiji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Foxo3a expression and acetylation regulate cancer cell growth and sensitivity to cisplatin</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2010-05</date><risdate>2010</risdate><volume>101</volume><issue>5</issue><spage>1177</spage><epage>1185</epage><pages>1177-1185</pages><issn>1347-9032</issn><issn>1349-7006</issn><eissn>1349-7006</eissn><abstract>Many advanced cancers receive cisplatin‐based chemotherapy. However, cisplatin resistance is a major obstacle for cancer chemotherapy. Foxo3a is a member of the Foxo transcription factor family, which modulates the expression of genes involved in DNA damage repair, apoptosis, and other cellular processes. In this study, we found that cisplatin‐resistant cells were more sensitive to the anticancer agent mithramycin than their parental cells, and had a decreased level of Foxo3a expression. Foxo3a knockdown increased cell proliferation and resistance to cisplatin. On the other hand, mithramycin stimulated Foxo3a expression through reactive oxygen species production and sensitized cells to cisplatin, which was abolished by Foxo3a knockdown, while the acetylation status of Foxo3a was decreased in response to cisplatin treatment and was lower in cisplatin‐resistant cells. Knockdown of Foxo3a‐associated acetyltransferase p300 promoted cancer‐cell growth and cisplatin resistance. In addition, non‐acetylation‐mimicking Foxo3a overexpression decreased cancer cell growth and sensitized cells to cisplatin less than wild‐type Foxo3a overexpression. The current work may contribute to the evaluation of the therapeutic potential of inducing the Foxo3a pathway and acetylating the Foxo3a transcription factor, and lead to the reevaluation of cancer treatments based on mithramycin.
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| subjects | Acetylation Antineoplastic Agents - pharmacology Biological and medical sciences Cell Line, Tumor Cell Proliferation Cisplatin - pharmacology Drug Resistance, Neoplasm Forkhead Box Protein O3 Forkhead Transcription Factors - analysis Forkhead Transcription Factors - physiology Humans Medical sciences Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology Original Plicamycin - pharmacology Reactive Oxygen Species - metabolism Tumors |
| title | Foxo3a expression and acetylation regulate cancer cell growth and sensitivity to cisplatin |
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