Triptolide sensitizes breast cancer cells to Doxorubicin through the DNA damage response inhibition
Triptolide is an active component from a Chinese herb, Tripterygium wilfordii which has been applied for treating immune‐related diseases over centuries. Recently, it was reported that a variety of cancer cell lines could be sensitized to DNA‐damage based chemotherapy drugs in combination with Tript...
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| Veröffentlicht in: | Molecular carcinogenesis 2018-06, Vol.57 (6), p.807-814 |
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| container_title | Molecular carcinogenesis |
| container_volume | 57 |
| creator | Deng, Yu Li, Fulun He, Pinglin Yang, Yafei Yang, Jin Zhang, Yamei Liu, Junying Tong, Yongping Li, Qingfeng Mei, Xian Shu, Zengyi Zhao, Qi |
| description | Triptolide is an active component from a Chinese herb, Tripterygium wilfordii which has been applied for treating immune‐related diseases over centuries. Recently, it was reported that a variety of cancer cell lines could be sensitized to DNA‐damage based chemotherapy drugs in combination with Triptolide treatment. In the present study, we show that a short time exposure (3 h) to Triptolide, which did not trigger apoptosis, could specifically increase breast cancer cells sensitivity to Doxorubicin rather than other chemotherapy drugs including Paclitaxel, Fluorouracil, and Mitomycin C. Further studies revealed Triptolide downregulated ATM expression and inhibited DNA damage response to DNA double‐ strand breaks. Moreover, the chemosensitization effect to Doxorubicin from Triptolide was attenuated by overexpression of ATM in breast cancer cells. Our findings suggest that Triptolide specifically chemosensitizes breast cancer cells to Doxorubicin prior to apoptosis initiation through downregulating ATM expression and inhibiting DNA damage response. |
| doi_str_mv | 10.1002/mc.22795 |
| format | Article |
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Recently, it was reported that a variety of cancer cell lines could be sensitized to DNA‐damage based chemotherapy drugs in combination with Triptolide treatment. In the present study, we show that a short time exposure (3 h) to Triptolide, which did not trigger apoptosis, could specifically increase breast cancer cells sensitivity to Doxorubicin rather than other chemotherapy drugs including Paclitaxel, Fluorouracil, and Mitomycin C. Further studies revealed Triptolide downregulated ATM expression and inhibited DNA damage response to DNA double‐ strand breaks. Moreover, the chemosensitization effect to Doxorubicin from Triptolide was attenuated by overexpression of ATM in breast cancer cells. Our findings suggest that Triptolide specifically chemosensitizes breast cancer cells to Doxorubicin prior to apoptosis initiation through downregulating ATM expression and inhibiting DNA damage response.</description><identifier>ISSN: 0899-1987</identifier><identifier>EISSN: 1098-2744</identifier><identifier>DOI: 10.1002/mc.22795</identifier><identifier>PMID: 29500880</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>5-Fluorouracil ; Apoptosis ; ATM ; Breast cancer ; Cancer therapies ; Chemosensitization ; Chemotherapy ; Deoxyribonucleic acid ; DNA ; DNA damage ; DNA damage response ; Doxorubicin ; Immunosuppressive agents ; Mitomycin C ; Paclitaxel ; Triptolide ; Tumor cell lines</subject><ispartof>Molecular carcinogenesis, 2018-06, Vol.57 (6), p.807-814</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4155-516b617a035737ceb011bfff14b46d4307a9a9fdcc3ac68a76cb20d91c492243</citedby><cites>FETCH-LOGICAL-c4155-516b617a035737ceb011bfff14b46d4307a9a9fdcc3ac68a76cb20d91c492243</cites><orcidid>0000-0003-4158-8966</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmc.22795$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmc.22795$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29500880$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deng, Yu</creatorcontrib><creatorcontrib>Li, Fulun</creatorcontrib><creatorcontrib>He, Pinglin</creatorcontrib><creatorcontrib>Yang, Yafei</creatorcontrib><creatorcontrib>Yang, Jin</creatorcontrib><creatorcontrib>Zhang, Yamei</creatorcontrib><creatorcontrib>Liu, Junying</creatorcontrib><creatorcontrib>Tong, Yongping</creatorcontrib><creatorcontrib>Li, Qingfeng</creatorcontrib><creatorcontrib>Mei, Xian</creatorcontrib><creatorcontrib>Shu, Zengyi</creatorcontrib><creatorcontrib>Zhao, Qi</creatorcontrib><title>Triptolide sensitizes breast cancer cells to Doxorubicin through the DNA damage response inhibition</title><title>Molecular carcinogenesis</title><addtitle>Mol Carcinog</addtitle><description>Triptolide is an active component from a Chinese herb, Tripterygium wilfordii which has been applied for treating immune‐related diseases over centuries. 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Our findings suggest that Triptolide specifically chemosensitizes breast cancer cells to Doxorubicin prior to apoptosis initiation through downregulating ATM expression and inhibiting DNA damage response.</description><subject>5-Fluorouracil</subject><subject>Apoptosis</subject><subject>ATM</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>Chemosensitization</subject><subject>Chemotherapy</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA damage response</subject><subject>Doxorubicin</subject><subject>Immunosuppressive agents</subject><subject>Mitomycin C</subject><subject>Paclitaxel</subject><subject>Triptolide</subject><subject>Tumor cell lines</subject><issn>0899-1987</issn><issn>1098-2744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kEFP2zAYhq2JaRSYxC9AlrhwSfnsOHF8rAobk8q49B7ZzhdqlMTFTgTs1-OubEhInN7Lo0evHkJOGcwZAL_s7ZxzqYovZMZAVRmXQhyQGVRKZUxV8pAcxfgAwJgs4Bs55KoAqCqYEbsObjv6zjVIIw7Rje4PRmoC6jhSqweLgVrsukhHT6_8sw-TcdYNdNwEP91v0iK9-r2gje71PdKAceuHiNQNG2eSzg8n5Guru4jf3_aYrH9cr5c32eru56_lYpVZwYoiK1hpSiY15IXMpUWT7pq2bZkwomxEDlIrrdrG2lzbstKytIZDo5gVinORH5OLvXYb_OOEcax7F3fX9YB-ijUHBrlMmVhCzz-gD34KQzqXqJyXlRC8ehfa4GMM2Nbb4HodXmoG9a573dv6b_eEnr0JJ9Nj8x_8FzoB2R54ch2-fCqqb5d74StDfIs-</recordid><startdate>201806</startdate><enddate>201806</enddate><creator>Deng, Yu</creator><creator>Li, Fulun</creator><creator>He, Pinglin</creator><creator>Yang, Yafei</creator><creator>Yang, Jin</creator><creator>Zhang, Yamei</creator><creator>Liu, Junying</creator><creator>Tong, Yongping</creator><creator>Li, Qingfeng</creator><creator>Mei, Xian</creator><creator>Shu, Zengyi</creator><creator>Zhao, Qi</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-4158-8966</orcidid></search><sort><creationdate>201806</creationdate><title>Triptolide sensitizes breast cancer cells to Doxorubicin through the DNA damage response inhibition</title><author>Deng, Yu ; 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Recently, it was reported that a variety of cancer cell lines could be sensitized to DNA‐damage based chemotherapy drugs in combination with Triptolide treatment. In the present study, we show that a short time exposure (3 h) to Triptolide, which did not trigger apoptosis, could specifically increase breast cancer cells sensitivity to Doxorubicin rather than other chemotherapy drugs including Paclitaxel, Fluorouracil, and Mitomycin C. Further studies revealed Triptolide downregulated ATM expression and inhibited DNA damage response to DNA double‐ strand breaks. Moreover, the chemosensitization effect to Doxorubicin from Triptolide was attenuated by overexpression of ATM in breast cancer cells. 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| subjects | 5-Fluorouracil Apoptosis ATM Breast cancer Cancer therapies Chemosensitization Chemotherapy Deoxyribonucleic acid DNA DNA damage DNA damage response Doxorubicin Immunosuppressive agents Mitomycin C Paclitaxel Triptolide Tumor cell lines |
| title | Triptolide sensitizes breast cancer cells to Doxorubicin through the DNA damage response inhibition |
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