Growth inhibitory effect of Cucurbitacin E on breast cancer cells
Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells. The inhibitory effect o...
Gespeichert in:
| Veröffentlicht in: | International journal of clinical and experimental pathology 2013-01, Vol.6 (9), p.1799-1805 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1805 |
|---|---|
| container_issue | 9 |
| container_start_page | 1799 |
| container_title | International journal of clinical and experimental pathology |
| container_volume | 6 |
| creator | Lan, Tian Wang, Linling Xu, Qian Liu, Weiguo Jin, Hongchuan Mao, Weimin Wang, Xian Wang, Xiaojia |
| description | Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells.
The inhibitory effect of CuE on proliferation of Bcap37 and MDA-MB-231 cells was assessed by MTT assay. The cell cycle distribution and cell apoptosis were determined by flow cytometry (FCM). The expression of pro-caspase 3, cleaved caspase 3, p21, p27 and the phosphorylation of signaling proteins was detected by Western Blotting.
CuE inhibited the growth of human breast cancer cells in a dose and time-dependent manner. FCM analysis showed that CuE induced G2/M phase arrest and cell apoptosis. CuE treatment promoted the cleavage of caspase 3 and upregulated p21 and p27. In addition, the phosphorylation of STAT3 but not ERK-1/2 was abrogated upon CuE treatment. Interestingly, losedose CuE significantly enhanced the growth inhibition induced by cisplatin. Conclusions Cucurbitacin E (CuE) could inhibit the growth of human breast cancer cells in vitro. CuE induced both apoptosis and cell cycle arrest probably through the inhibition of STAT3 function. Lose-dose CuE significantly enhanced the growth inhibitory effect of cisplatin on breast cancer cells, further indicating the potential clinical values of CuE for the prevention or treatment of human breast cancer. |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3759486</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>24040444</sourcerecordid><originalsourceid>FETCH-LOGICAL-p266t-3b55b7191d4470807f52d61c22176ab51f607d7146a6c43d4b39800919a352893</originalsourceid><addsrcrecordid>eNpVkNtKxDAYhIMg7rr6CpIXKOSc5kZYyroKC97odUnSxEa6SUlTZd_eggdWBuaHGf7vYi7AGisqKiIIX4HraXpHSGDC0BVYLb6IsTXY7nP6LD0MsQ8mlJRP0HnvbIHJw2a2c15SbUOEO5giNNnpqUCro3UZWjcM0w249HqY3O3P3YDXh91L81gdnvdPzfZQjUSIUlHDuZFY4Y4xiWokPSedwJYQLIU2HHuBZCcxE1pYRjtmqKoRUlhpykmt6Abcf3PH2RxdZ10sWQ_tmMNR51ObdGj_NzH07Vv6aKnkitViAdydA_4-f8egX3-PWdQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Growth inhibitory effect of Cucurbitacin E on breast cancer cells</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Lan, Tian ; Wang, Linling ; Xu, Qian ; Liu, Weiguo ; Jin, Hongchuan ; Mao, Weimin ; Wang, Xian ; Wang, Xiaojia</creator><creatorcontrib>Lan, Tian ; Wang, Linling ; Xu, Qian ; Liu, Weiguo ; Jin, Hongchuan ; Mao, Weimin ; Wang, Xian ; Wang, Xiaojia</creatorcontrib><description>Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells.
The inhibitory effect of CuE on proliferation of Bcap37 and MDA-MB-231 cells was assessed by MTT assay. The cell cycle distribution and cell apoptosis were determined by flow cytometry (FCM). The expression of pro-caspase 3, cleaved caspase 3, p21, p27 and the phosphorylation of signaling proteins was detected by Western Blotting.
CuE inhibited the growth of human breast cancer cells in a dose and time-dependent manner. FCM analysis showed that CuE induced G2/M phase arrest and cell apoptosis. CuE treatment promoted the cleavage of caspase 3 and upregulated p21 and p27. In addition, the phosphorylation of STAT3 but not ERK-1/2 was abrogated upon CuE treatment. Interestingly, losedose CuE significantly enhanced the growth inhibition induced by cisplatin. Conclusions Cucurbitacin E (CuE) could inhibit the growth of human breast cancer cells in vitro. CuE induced both apoptosis and cell cycle arrest probably through the inhibition of STAT3 function. Lose-dose CuE significantly enhanced the growth inhibitory effect of cisplatin on breast cancer cells, further indicating the potential clinical values of CuE for the prevention or treatment of human breast cancer.</description><identifier>EISSN: 1936-2625</identifier><identifier>PMID: 24040444</identifier><language>eng</language><publisher>United States: e-Century Publishing Corporation</publisher><subject>Antineoplastic Agents, Phytogenic - pharmacology ; Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Apoptosis - drug effects ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Caspase 3 - metabolism ; Cell Cycle Checkpoints - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cisplatin - pharmacology ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Cyclin-Dependent Kinase Inhibitor p27 - metabolism ; Dose-Response Relationship, Drug ; Drug Synergism ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Female ; Humans ; Original ; Phosphorylation ; Signal Transduction - drug effects ; STAT3 Transcription Factor - metabolism ; Time Factors ; Triterpenes - pharmacology</subject><ispartof>International journal of clinical and experimental pathology, 2013-01, Vol.6 (9), p.1799-1805</ispartof><rights>IJCEP Copyright © 2013 2013</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759486/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759486/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24040444$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lan, Tian</creatorcontrib><creatorcontrib>Wang, Linling</creatorcontrib><creatorcontrib>Xu, Qian</creatorcontrib><creatorcontrib>Liu, Weiguo</creatorcontrib><creatorcontrib>Jin, Hongchuan</creatorcontrib><creatorcontrib>Mao, Weimin</creatorcontrib><creatorcontrib>Wang, Xian</creatorcontrib><creatorcontrib>Wang, Xiaojia</creatorcontrib><title>Growth inhibitory effect of Cucurbitacin E on breast cancer cells</title><title>International journal of clinical and experimental pathology</title><addtitle>Int J Clin Exp Pathol</addtitle><description>Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells.
The inhibitory effect of CuE on proliferation of Bcap37 and MDA-MB-231 cells was assessed by MTT assay. The cell cycle distribution and cell apoptosis were determined by flow cytometry (FCM). The expression of pro-caspase 3, cleaved caspase 3, p21, p27 and the phosphorylation of signaling proteins was detected by Western Blotting.
CuE inhibited the growth of human breast cancer cells in a dose and time-dependent manner. FCM analysis showed that CuE induced G2/M phase arrest and cell apoptosis. CuE treatment promoted the cleavage of caspase 3 and upregulated p21 and p27. In addition, the phosphorylation of STAT3 but not ERK-1/2 was abrogated upon CuE treatment. Interestingly, losedose CuE significantly enhanced the growth inhibition induced by cisplatin. Conclusions Cucurbitacin E (CuE) could inhibit the growth of human breast cancer cells in vitro. CuE induced both apoptosis and cell cycle arrest probably through the inhibition of STAT3 function. Lose-dose CuE significantly enhanced the growth inhibitory effect of cisplatin on breast cancer cells, further indicating the potential clinical values of CuE for the prevention or treatment of human breast cancer.</description><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cisplatin - pharmacology</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Synergism</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Original</subject><subject>Phosphorylation</subject><subject>Signal Transduction - drug effects</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Time Factors</subject><subject>Triterpenes - pharmacology</subject><issn>1936-2625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkNtKxDAYhIMg7rr6CpIXKOSc5kZYyroKC97odUnSxEa6SUlTZd_eggdWBuaHGf7vYi7AGisqKiIIX4HraXpHSGDC0BVYLb6IsTXY7nP6LD0MsQ8mlJRP0HnvbIHJw2a2c15SbUOEO5giNNnpqUCro3UZWjcM0w249HqY3O3P3YDXh91L81gdnvdPzfZQjUSIUlHDuZFY4Y4xiWokPSedwJYQLIU2HHuBZCcxE1pYRjtmqKoRUlhpykmt6Abcf3PH2RxdZ10sWQ_tmMNR51ObdGj_NzH07Vv6aKnkitViAdydA_4-f8egX3-PWdQ</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>Lan, Tian</creator><creator>Wang, Linling</creator><creator>Xu, Qian</creator><creator>Liu, Weiguo</creator><creator>Jin, Hongchuan</creator><creator>Mao, Weimin</creator><creator>Wang, Xian</creator><creator>Wang, Xiaojia</creator><general>e-Century Publishing Corporation</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>5PM</scope></search><sort><creationdate>20130101</creationdate><title>Growth inhibitory effect of Cucurbitacin E on breast cancer cells</title><author>Lan, Tian ; Wang, Linling ; Xu, Qian ; Liu, Weiguo ; Jin, Hongchuan ; Mao, Weimin ; Wang, Xian ; Wang, Xiaojia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p266t-3b55b7191d4470807f52d61c22176ab51f607d7146a6c43d4b39800919a352893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Antineoplastic Combined Chemotherapy Protocols - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cisplatin - pharmacology</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Synergism</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Original</topic><topic>Phosphorylation</topic><topic>Signal Transduction - drug effects</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Time Factors</topic><topic>Triterpenes - pharmacology</topic><toplevel>online_resources</toplevel><creatorcontrib>Lan, Tian</creatorcontrib><creatorcontrib>Wang, Linling</creatorcontrib><creatorcontrib>Xu, Qian</creatorcontrib><creatorcontrib>Liu, Weiguo</creatorcontrib><creatorcontrib>Jin, Hongchuan</creatorcontrib><creatorcontrib>Mao, Weimin</creatorcontrib><creatorcontrib>Wang, Xian</creatorcontrib><creatorcontrib>Wang, Xiaojia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of clinical and experimental pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lan, Tian</au><au>Wang, Linling</au><au>Xu, Qian</au><au>Liu, Weiguo</au><au>Jin, Hongchuan</au><au>Mao, Weimin</au><au>Wang, Xian</au><au>Wang, Xiaojia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Growth inhibitory effect of Cucurbitacin E on breast cancer cells</atitle><jtitle>International journal of clinical and experimental pathology</jtitle><addtitle>Int J Clin Exp Pathol</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>6</volume><issue>9</issue><spage>1799</spage><epage>1805</epage><pages>1799-1805</pages><eissn>1936-2625</eissn><abstract>Due its inhibitory effects on chemical carcinogenesis and inflammation, Cucurbitacins have been proposed as an effective agent for the prevention or treatment of human cancers. In this study, we aimed to explore the effect of Cucurbitacin E (CuE) on human breast cancer cells.
The inhibitory effect of CuE on proliferation of Bcap37 and MDA-MB-231 cells was assessed by MTT assay. The cell cycle distribution and cell apoptosis were determined by flow cytometry (FCM). The expression of pro-caspase 3, cleaved caspase 3, p21, p27 and the phosphorylation of signaling proteins was detected by Western Blotting.
CuE inhibited the growth of human breast cancer cells in a dose and time-dependent manner. FCM analysis showed that CuE induced G2/M phase arrest and cell apoptosis. CuE treatment promoted the cleavage of caspase 3 and upregulated p21 and p27. In addition, the phosphorylation of STAT3 but not ERK-1/2 was abrogated upon CuE treatment. Interestingly, losedose CuE significantly enhanced the growth inhibition induced by cisplatin. Conclusions Cucurbitacin E (CuE) could inhibit the growth of human breast cancer cells in vitro. CuE induced both apoptosis and cell cycle arrest probably through the inhibition of STAT3 function. Lose-dose CuE significantly enhanced the growth inhibitory effect of cisplatin on breast cancer cells, further indicating the potential clinical values of CuE for the prevention or treatment of human breast cancer.</abstract><cop>United States</cop><pub>e-Century Publishing Corporation</pub><pmid>24040444</pmid><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | EISSN: 1936-2625 |
| ispartof | International journal of clinical and experimental pathology, 2013-01, Vol.6 (9), p.1799-1805 |
| issn | 1936-2625 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3759486 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Antineoplastic Agents, Phytogenic - pharmacology Antineoplastic Combined Chemotherapy Protocols - pharmacology Apoptosis - drug effects Breast Neoplasms - metabolism Breast Neoplasms - pathology Caspase 3 - metabolism Cell Cycle Checkpoints - drug effects Cell Line, Tumor Cell Proliferation - drug effects Cisplatin - pharmacology Cyclin-Dependent Kinase Inhibitor p21 - metabolism Cyclin-Dependent Kinase Inhibitor p27 - metabolism Dose-Response Relationship, Drug Drug Synergism Extracellular Signal-Regulated MAP Kinases - metabolism Female Humans Original Phosphorylation Signal Transduction - drug effects STAT3 Transcription Factor - metabolism Time Factors Triterpenes - pharmacology |
| title | Growth inhibitory effect of Cucurbitacin E on breast cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T03%3A01%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Growth%20inhibitory%20effect%20of%20Cucurbitacin%20E%20on%20breast%20cancer%20cells&rft.jtitle=International%20journal%20of%20clinical%20and%20experimental%20pathology&rft.au=Lan,%20Tian&rft.date=2013-01-01&rft.volume=6&rft.issue=9&rft.spage=1799&rft.epage=1805&rft.pages=1799-1805&rft.eissn=1936-2625&rft_id=info:doi/&rft_dat=%3Cpubmed%3E24040444%3C/pubmed%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/24040444&rfr_iscdi=true |