Tetramethylpyrazine reverses multidrug resistance in breast cancer cells through regulating the expression and function of P-glycoprotein
Tumor multidrug resistance (MDR) has become the major obstacle to cancer chemotherapy. Recent studies suggest that tetramethylpyrazine (TMP) could reverse tumor MDR although the mechanism by which TMP overcomes tumor MDR remains elusive. Therefore, in this study, we examined the effects of TMP on MD...
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| Veröffentlicht in: | Medical oncology (Northwood, London, England) London, England), 2012-06, Vol.29 (2), p.534-538 |
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| creator | Zhang, Yinxu Liu, Xiaomei Zuo, Teng Liu, Yu Zhang, Jun Hua |
| description | Tumor multidrug resistance (MDR) has become the major obstacle to cancer chemotherapy. Recent studies suggest that tetramethylpyrazine (TMP) could reverse tumor MDR although the mechanism by which TMP overcomes tumor MDR remains elusive. Therefore, in this study, we examined the effects of TMP on MDR in drug-resistant breast cancer cells and investigated the underlying mechanisms. MCF-7 cells and the derived P-glycoprotein (Pgp) overexpressing MCF-7/dox cells were treated with TMP, and their growth was examined by MTT assay. Doxorubicin accumulation in the cells was evaluated by flow cytometry, and the expression of Pgp was detected by Western blot and RT–PCR analysis. The results showed that TMP increased the intracellular concentration of doxorubicin and inhibited Pgp-mediated efflux of doxorubicin in a dose-dependent manner. Moreover, TMP inhibited the ATPase activity of P-gp and suppressed the expression of Pgp in MCF-7/dox cells. Taken together, these data suggest that TMP has potential application in the treatment of chemotherapy-resistant breast cancer. |
| doi_str_mv | 10.1007/s12032-011-9950-8 |
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Recent studies suggest that tetramethylpyrazine (TMP) could reverse tumor MDR although the mechanism by which TMP overcomes tumor MDR remains elusive. Therefore, in this study, we examined the effects of TMP on MDR in drug-resistant breast cancer cells and investigated the underlying mechanisms. MCF-7 cells and the derived P-glycoprotein (Pgp) overexpressing MCF-7/dox cells were treated with TMP, and their growth was examined by MTT assay. Doxorubicin accumulation in the cells was evaluated by flow cytometry, and the expression of Pgp was detected by Western blot and RT–PCR analysis. The results showed that TMP increased the intracellular concentration of doxorubicin and inhibited Pgp-mediated efflux of doxorubicin in a dose-dependent manner. Moreover, TMP inhibited the ATPase activity of P-gp and suppressed the expression of Pgp in MCF-7/dox cells. 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Recent studies suggest that tetramethylpyrazine (TMP) could reverse tumor MDR although the mechanism by which TMP overcomes tumor MDR remains elusive. Therefore, in this study, we examined the effects of TMP on MDR in drug-resistant breast cancer cells and investigated the underlying mechanisms. MCF-7 cells and the derived P-glycoprotein (Pgp) overexpressing MCF-7/dox cells were treated with TMP, and their growth was examined by MTT assay. Doxorubicin accumulation in the cells was evaluated by flow cytometry, and the expression of Pgp was detected by Western blot and RT–PCR analysis. The results showed that TMP increased the intracellular concentration of doxorubicin and inhibited Pgp-mediated efflux of doxorubicin in a dose-dependent manner. Moreover, TMP inhibited the ATPase activity of P-gp and suppressed the expression of Pgp in MCF-7/dox cells. 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Liu, Xiaomei ; Zuo, Teng ; Liu, Yu ; Zhang, Jun Hua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-85b5e3b2b08fd2cea31f22d8f434353f9df2f209da9562b79dc20d1f5c81b8ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenosine Triphosphatases - metabolism</topic><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>ATP Binding Cassette Transporter, Sub-Family B - genetics</topic><topic>ATP Binding Cassette Transporter, Sub-Family B - metabolism</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cell Proliferation</topic><topic>Doxorubicin - pharmacology</topic><topic>Drug Resistance, Multiple - drug effects</topic><topic>Drug Resistance, Neoplasm - drug effects</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Pyrazines - pharmacology</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Tumor Cells, Cultured</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yinxu</creatorcontrib><creatorcontrib>Liu, Xiaomei</creatorcontrib><creatorcontrib>Zuo, Teng</creatorcontrib><creatorcontrib>Liu, Yu</creatorcontrib><creatorcontrib>Zhang, Jun Hua</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Medical oncology (Northwood, London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yinxu</au><au>Liu, Xiaomei</au><au>Zuo, Teng</au><au>Liu, Yu</au><au>Zhang, Jun Hua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tetramethylpyrazine reverses multidrug resistance in breast cancer cells through regulating the expression and function of P-glycoprotein</atitle><jtitle>Medical oncology (Northwood, London, England)</jtitle><stitle>Med Oncol</stitle><addtitle>Med Oncol</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>29</volume><issue>2</issue><spage>534</spage><epage>538</epage><pages>534-538</pages><issn>1357-0560</issn><eissn>1559-131X</eissn><coden>MONCEZ</coden><abstract>Tumor multidrug resistance (MDR) has become the major obstacle to cancer chemotherapy. Recent studies suggest that tetramethylpyrazine (TMP) could reverse tumor MDR although the mechanism by which TMP overcomes tumor MDR remains elusive. Therefore, in this study, we examined the effects of TMP on MDR in drug-resistant breast cancer cells and investigated the underlying mechanisms. MCF-7 cells and the derived P-glycoprotein (Pgp) overexpressing MCF-7/dox cells were treated with TMP, and their growth was examined by MTT assay. Doxorubicin accumulation in the cells was evaluated by flow cytometry, and the expression of Pgp was detected by Western blot and RT–PCR analysis. The results showed that TMP increased the intracellular concentration of doxorubicin and inhibited Pgp-mediated efflux of doxorubicin in a dose-dependent manner. Moreover, TMP inhibited the ATPase activity of P-gp and suppressed the expression of Pgp in MCF-7/dox cells. Taken together, these data suggest that TMP has potential application in the treatment of chemotherapy-resistant breast cancer.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21562851</pmid><doi>10.1007/s12032-011-9950-8</doi><tpages>5</tpages></addata></record> |
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| subjects | Adenosine Triphosphatases - metabolism Antibiotics, Antineoplastic - pharmacology ATP Binding Cassette Transporter, Sub-Family B - genetics ATP Binding Cassette Transporter, Sub-Family B - metabolism Blotting, Western Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Cell Proliferation Doxorubicin - pharmacology Drug Resistance, Multiple - drug effects Drug Resistance, Neoplasm - drug effects Female Flow Cytometry Gene Expression Regulation, Neoplastic - drug effects Hematology Humans Internal Medicine Medicine Medicine & Public Health Oncology Original Paper Pathology Pyrazines - pharmacology Real-Time Polymerase Chain Reaction RNA, Messenger - genetics Tumor Cells, Cultured Vasodilator Agents - pharmacology |
| title | Tetramethylpyrazine reverses multidrug resistance in breast cancer cells through regulating the expression and function of P-glycoprotein |
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