Cucurbitacin B inhibits tumor angiogenesis by triggering the mitochondrial signaling pathway in endothelial cells
Cucurbitacin B (CuB), the active component of a traditional Chinese herbal medicine, Pedicellus Melo, has been shown to exhibit antitumor and anti-inflammation effects, but its role in tumor angiogenesis, the key step involved in tumor growth and metastasis, and the involved molecular mechanism are...
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Veröffentlicht in: | International journal of molecular medicine 2018-08, Vol.42 (2), p.1018-1025 |
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creator | Piao, Xian-Mei Gao, Feng Zhu, Jiu-Xin Wang, Li-Juan Zhao, Xin Li, Xin Sheng, Miao-Miao Zhang, Yan |
description | Cucurbitacin B (CuB), the active component of a traditional Chinese herbal medicine, Pedicellus Melo, has been shown to exhibit antitumor and anti-inflammation effects, but its role in tumor angiogenesis, the key step involved in tumor growth and metastasis, and the involved molecular mechanism are unknown. Tumor angiogenesis is one of the hallmarks of the development in malignant neoplasias and metastasis. Effective targeting of tumor angiogenesis is a key area of interest for cancer therapy. Here, we demonstrated that CuB significantly inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, migration, tubulogenesis in vitro, and blocked angiogenesis in chick embryo chorioallantoic membrane (CAM) assay in vivo. Furthermore, CuB induced HUVEC apoptosis and may induce apoptosis by triggering the mitochondrial apoptotic pathway. Finally, we found that CuB inhibiting angiogenesis was associated with inhibition of the activity of vascular endothelial growth factor receptor 2 (VEGFR2). Our investigations suggested that CuB was a potential drug candidate for angiogenesis related diseases. |
doi_str_mv | 10.3892/ijmm.2018.3647 |
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Tumor angiogenesis is one of the hallmarks of the development in malignant neoplasias and metastasis. Effective targeting of tumor angiogenesis is a key area of interest for cancer therapy. Here, we demonstrated that CuB significantly inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, migration, tubulogenesis in vitro, and blocked angiogenesis in chick embryo chorioallantoic membrane (CAM) assay in vivo. Furthermore, CuB induced HUVEC apoptosis and may induce apoptosis by triggering the mitochondrial apoptotic pathway. Finally, we found that CuB inhibiting angiogenesis was associated with inhibition of the activity of vascular endothelial growth factor receptor 2 (VEGFR2). Our investigations suggested that CuB was a potential drug candidate for angiogenesis related diseases.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2018.3647</identifier><identifier>PMID: 29717773</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Angiogenesis ; Apoptosis ; Cell cycle ; Cell growth ; Cellular signal transduction ; Diabetic retinopathy ; Drug dosages ; Experiments ; Health aspects ; Immunoglobulins ; Kinases ; Lung cancer ; Muskmelon ; Neovascularization ; Plant products ; Studies ; Vascular endothelial growth factor</subject><ispartof>International journal of molecular medicine, 2018-08, Vol.42 (2), p.1018-1025</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-92a45d4950b9c0378063a2c9081b5ba513e8ecc092bafab57cd83eca23cf720b3</citedby><cites>FETCH-LOGICAL-c391t-92a45d4950b9c0378063a2c9081b5ba513e8ecc092bafab57cd83eca23cf720b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29717773$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Piao, Xian-Mei</creatorcontrib><creatorcontrib>Gao, Feng</creatorcontrib><creatorcontrib>Zhu, Jiu-Xin</creatorcontrib><creatorcontrib>Wang, Li-Juan</creatorcontrib><creatorcontrib>Zhao, Xin</creatorcontrib><creatorcontrib>Li, Xin</creatorcontrib><creatorcontrib>Sheng, Miao-Miao</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><title>Cucurbitacin B inhibits tumor angiogenesis by triggering the mitochondrial signaling pathway in endothelial cells</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Cucurbitacin B (CuB), the active component of a traditional Chinese herbal medicine, Pedicellus Melo, has been shown to exhibit antitumor and anti-inflammation effects, but its role in tumor angiogenesis, the key step involved in tumor growth and metastasis, and the involved molecular mechanism are unknown. Tumor angiogenesis is one of the hallmarks of the development in malignant neoplasias and metastasis. Effective targeting of tumor angiogenesis is a key area of interest for cancer therapy. Here, we demonstrated that CuB significantly inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, migration, tubulogenesis in vitro, and blocked angiogenesis in chick embryo chorioallantoic membrane (CAM) assay in vivo. Furthermore, CuB induced HUVEC apoptosis and may induce apoptosis by triggering the mitochondrial apoptotic pathway. Finally, we found that CuB inhibiting angiogenesis was associated with inhibition of the activity of vascular endothelial growth factor receptor 2 (VEGFR2). Our investigations suggested that CuB was a potential drug candidate for angiogenesis related diseases.</description><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cellular signal transduction</subject><subject>Diabetic retinopathy</subject><subject>Drug dosages</subject><subject>Experiments</subject><subject>Health aspects</subject><subject>Immunoglobulins</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Muskmelon</subject><subject>Neovascularization</subject><subject>Plant products</subject><subject>Studies</subject><subject>Vascular endothelial growth factor</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpFkctLxDAQxoMorq-rRwl47ppH0zRHXXyB4EXBW0jStJulTdYkRfa_t2V9nGaG-c03w3wAXGK0pLUgN24zDEuCcL2kVckPwAnmAhekLD8OpxwjXlDOqgU4TWmDEGGlqI_BggiOOef0BHyuRjNG7bIyzsM76PzaTVWCeRxChMp3LnTW2-QS1DuYo-s6G53vYF5bOLgczDr4JjrVw-Q6r_q5t1V5_aV2kxq0vgkT2s-AsX2fzsFRq_pkL37iGXh_uH9bPRUvr4_Pq9uXwlCBcyGIKllTCoa0MIjyGlVUESNQjTXTimFqa2sMEkSrVmnGTVNTaxShpuUEaXoGrve62xg-R5uy3IQxTgcmSZCoSFVXAv1TneqtdL4NOSozuGTkLWMUk4ohMlHLPWViSCnaVm6jG1TcSYzk7IOcfZCzD3L2YRq4-lk-6sE2f_jv4-k3gt2FdA</recordid><startdate>20180801</startdate><enddate>20180801</enddate><creator>Piao, Xian-Mei</creator><creator>Gao, Feng</creator><creator>Zhu, Jiu-Xin</creator><creator>Wang, Li-Juan</creator><creator>Zhao, Xin</creator><creator>Li, Xin</creator><creator>Sheng, Miao-Miao</creator><creator>Zhang, Yan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20180801</creationdate><title>Cucurbitacin B inhibits tumor angiogenesis by triggering the mitochondrial signaling pathway in endothelial cells</title><author>Piao, Xian-Mei ; 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Tumor angiogenesis is one of the hallmarks of the development in malignant neoplasias and metastasis. Effective targeting of tumor angiogenesis is a key area of interest for cancer therapy. Here, we demonstrated that CuB significantly inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, migration, tubulogenesis in vitro, and blocked angiogenesis in chick embryo chorioallantoic membrane (CAM) assay in vivo. Furthermore, CuB induced HUVEC apoptosis and may induce apoptosis by triggering the mitochondrial apoptotic pathway. Finally, we found that CuB inhibiting angiogenesis was associated with inhibition of the activity of vascular endothelial growth factor receptor 2 (VEGFR2). Our investigations suggested that CuB was a potential drug candidate for angiogenesis related diseases.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29717773</pmid><doi>10.3892/ijmm.2018.3647</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Angiogenesis Apoptosis Cell cycle Cell growth Cellular signal transduction Diabetic retinopathy Drug dosages Experiments Health aspects Immunoglobulins Kinases Lung cancer Muskmelon Neovascularization Plant products Studies Vascular endothelial growth factor |
title | Cucurbitacin B inhibits tumor angiogenesis by triggering the mitochondrial signaling pathway in endothelial cells |
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