Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells
This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-overexpressing MDA-MB-453 breast cancer cells. The antiproliferative effects of apigenin were examined by proliferation and MTT assays. The effect of apigenin on apoptotic molecules was determined by western bl...
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| Veröffentlicht in: | Anticancer research 2014-06, Vol.34 (6), p.2869-2882 |
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| container_title | Anticancer research |
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| creator | Seo, Hye-Sook Ku, Jin Mo Choi, Han-Seok Woo, Jong-Kyu Jang, Bo-Hyoung Shin, Yong Cheol Ko, Seong-Gyu |
| description | This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-overexpressing MDA-MB-453 breast cancer cells.
The antiproliferative effects of apigenin were examined by proliferation and MTT assays. The effect of apigenin on apoptotic molecules was determined by western blotting. RT-PCR was performed to measure mRNA levels of HIF-1α and VEGF. ELISA assay was performed to measure intracellular VEGF levels. Immunocytochemistry was performed to evaluate nuclear STAT3 level.
Apigenin inhibited the proliferation of MDA-MB-453 cells. Apigenin up-regulated the levels of cleaved caspase-8 and caspase-3, and induced the cleavage of PARP. Apigenin induced extrinsic apoptosis and blocked the activation (phosphorylation) of JAK2 and STAT3. Apigenin inhibited CoCl2-induced VEGF secretion and decreased the nuclear staining of STAT3.
Apigenin exerts its antiproliferative activity by inhibiting STAT3 signaling. Apigenin could serve as a useful compound to prevent or treat HER2-overexpressing breast cancer. |
| format | Article |
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The antiproliferative effects of apigenin were examined by proliferation and MTT assays. The effect of apigenin on apoptotic molecules was determined by western blotting. RT-PCR was performed to measure mRNA levels of HIF-1α and VEGF. ELISA assay was performed to measure intracellular VEGF levels. Immunocytochemistry was performed to evaluate nuclear STAT3 level.
Apigenin inhibited the proliferation of MDA-MB-453 cells. Apigenin up-regulated the levels of cleaved caspase-8 and caspase-3, and induced the cleavage of PARP. Apigenin induced extrinsic apoptosis and blocked the activation (phosphorylation) of JAK2 and STAT3. Apigenin inhibited CoCl2-induced VEGF secretion and decreased the nuclear staining of STAT3.
Apigenin exerts its antiproliferative activity by inhibiting STAT3 signaling. Apigenin could serve as a useful compound to prevent or treat HER2-overexpressing breast cancer.</description><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 24922650</identifier><language>eng</language><publisher>Greece</publisher><subject>Apigenin - pharmacology ; Apoptosis - drug effects ; Blotting, Western ; Breast Neoplasms - drug therapy ; Breast Neoplasms - enzymology ; Breast Neoplasms - pathology ; Caspases - genetics ; Caspases - metabolism ; Cell Cycle - drug effects ; Cell Proliferation - drug effects ; Female ; Flow Cytometry ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Immunoenzyme Techniques ; Phosphorylation - drug effects ; Real-Time Polymerase Chain Reaction ; Receptor, ErbB-2 - genetics ; Receptor, ErbB-2 - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; STAT3 Transcription Factor - antagonists & inhibitors ; STAT3 Transcription Factor - genetics ; STAT3 Transcription Factor - metabolism ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Anticancer research, 2014-06, Vol.34 (6), p.2869-2882</ispartof><rights>Copyright© 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24922650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seo, Hye-Sook</creatorcontrib><creatorcontrib>Ku, Jin Mo</creatorcontrib><creatorcontrib>Choi, Han-Seok</creatorcontrib><creatorcontrib>Woo, Jong-Kyu</creatorcontrib><creatorcontrib>Jang, Bo-Hyoung</creatorcontrib><creatorcontrib>Shin, Yong Cheol</creatorcontrib><creatorcontrib>Ko, Seong-Gyu</creatorcontrib><title>Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-overexpressing MDA-MB-453 breast cancer cells.
The antiproliferative effects of apigenin were examined by proliferation and MTT assays. The effect of apigenin on apoptotic molecules was determined by western blotting. RT-PCR was performed to measure mRNA levels of HIF-1α and VEGF. ELISA assay was performed to measure intracellular VEGF levels. Immunocytochemistry was performed to evaluate nuclear STAT3 level.
Apigenin inhibited the proliferation of MDA-MB-453 cells. Apigenin up-regulated the levels of cleaved caspase-8 and caspase-3, and induced the cleavage of PARP. Apigenin induced extrinsic apoptosis and blocked the activation (phosphorylation) of JAK2 and STAT3. Apigenin inhibited CoCl2-induced VEGF secretion and decreased the nuclear staining of STAT3.
Apigenin exerts its antiproliferative activity by inhibiting STAT3 signaling. Apigenin could serve as a useful compound to prevent or treat HER2-overexpressing breast cancer.</description><subject>Apigenin - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - pathology</subject><subject>Caspases - genetics</subject><subject>Caspases - metabolism</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Immunoenzyme Techniques</subject><subject>Phosphorylation - drug effects</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>STAT3 Transcription Factor - antagonists & inhibitors</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Tumor Cells, Cultured</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kE1OwzAQhSMkREvhCshLNpbiv6RellJopVZIUNaRE0-KUeqYjIPoDTg2iYDVzDd6895ozpIpyzWjuRLpJLlEfE_TLNNzcZFMuNScZyqdJt8bb_squtaTtiaVwWAQqIUA3oKPxIQ2xBYdkvI0gDuAd37snX9zpYvOH8jLfrEXBN3Bm2bkQbBePXPafkIHX6EDxHG8u1_Q3R2VSpCyA4NxiPMVdKSCpsGr5Lw2DcL1X50lrw-r_XJNt0-Pm-ViSwNnLFI5t6wGqErQVVbXpZW5UFkFwAYUTCojaiVNKsost1xLDfk8FWCFGHa0ycQsuf31DV370QPG4uhwvMB4aHssmBr8uGaaDdKbP2lfHsEWoXNH052K_--JH6bRa_M</recordid><startdate>201406</startdate><enddate>201406</enddate><creator>Seo, Hye-Sook</creator><creator>Ku, Jin Mo</creator><creator>Choi, Han-Seok</creator><creator>Woo, Jong-Kyu</creator><creator>Jang, Bo-Hyoung</creator><creator>Shin, Yong Cheol</creator><creator>Ko, Seong-Gyu</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>201406</creationdate><title>Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells</title><author>Seo, Hye-Sook ; Ku, Jin Mo ; Choi, Han-Seok ; Woo, Jong-Kyu ; Jang, Bo-Hyoung ; Shin, Yong Cheol ; Ko, Seong-Gyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p211t-48d1feecbe9c6ffbd47356cee1c6f3145a3f54a03b67d2949e7803ed33ecb9a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Apigenin - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - enzymology</topic><topic>Breast Neoplasms - pathology</topic><topic>Caspases - genetics</topic><topic>Caspases - metabolism</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Immunoenzyme Techniques</topic><topic>Phosphorylation - drug effects</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>STAT3 Transcription Factor - antagonists & inhibitors</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Tumor Cells, Cultured</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seo, Hye-Sook</creatorcontrib><creatorcontrib>Ku, Jin Mo</creatorcontrib><creatorcontrib>Choi, Han-Seok</creatorcontrib><creatorcontrib>Woo, Jong-Kyu</creatorcontrib><creatorcontrib>Jang, Bo-Hyoung</creatorcontrib><creatorcontrib>Shin, Yong Cheol</creatorcontrib><creatorcontrib>Ko, Seong-Gyu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seo, Hye-Sook</au><au>Ku, Jin Mo</au><au>Choi, Han-Seok</au><au>Woo, Jong-Kyu</au><au>Jang, Bo-Hyoung</au><au>Shin, Yong Cheol</au><au>Ko, Seong-Gyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2014-06</date><risdate>2014</risdate><volume>34</volume><issue>6</issue><spage>2869</spage><epage>2882</epage><pages>2869-2882</pages><eissn>1791-7530</eissn><abstract>This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-overexpressing MDA-MB-453 breast cancer cells.
The antiproliferative effects of apigenin were examined by proliferation and MTT assays. The effect of apigenin on apoptotic molecules was determined by western blotting. RT-PCR was performed to measure mRNA levels of HIF-1α and VEGF. ELISA assay was performed to measure intracellular VEGF levels. Immunocytochemistry was performed to evaluate nuclear STAT3 level.
Apigenin inhibited the proliferation of MDA-MB-453 cells. Apigenin up-regulated the levels of cleaved caspase-8 and caspase-3, and induced the cleavage of PARP. Apigenin induced extrinsic apoptosis and blocked the activation (phosphorylation) of JAK2 and STAT3. Apigenin inhibited CoCl2-induced VEGF secretion and decreased the nuclear staining of STAT3.
Apigenin exerts its antiproliferative activity by inhibiting STAT3 signaling. Apigenin could serve as a useful compound to prevent or treat HER2-overexpressing breast cancer.</abstract><cop>Greece</cop><pmid>24922650</pmid><tpages>14</tpages></addata></record> |
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| subjects | Apigenin - pharmacology Apoptosis - drug effects Blotting, Western Breast Neoplasms - drug therapy Breast Neoplasms - enzymology Breast Neoplasms - pathology Caspases - genetics Caspases - metabolism Cell Cycle - drug effects Cell Proliferation - drug effects Female Flow Cytometry Humans Hypoxia-Inducible Factor 1, alpha Subunit - genetics Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Immunoenzyme Techniques Phosphorylation - drug effects Real-Time Polymerase Chain Reaction Receptor, ErbB-2 - genetics Receptor, ErbB-2 - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics STAT3 Transcription Factor - antagonists & inhibitors STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Tumor Cells, Cultured Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism |
| title | Induction of caspase-dependent apoptosis by apigenin by inhibiting STAT3 signaling in HER2-overexpressing MDA-MB-453 breast cancer cells |
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