All-trans retinoic acid suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and metastasis in esophageal squamous cell carcinoma
Esophageal squamous cell carcinoma (ESCC) is the second common cancer in Henan province and is well-known for aggressiveness and dismal prognosis. Adjuvant therapies, chemotherapy, radiotherapy and endoscopic treatment have not improved survival rates in patients with late stage esophageal carcinoma...
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| Veröffentlicht in: | PloS one 2017-04, Vol.12 (4), p.e0174555 |
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| creator | Li, Na Lu, Yanjuan Li, Daoming Zheng, Xiangyu Lian, Jingyao Li, Shanshan Cui, Huijuan Zhang, Linda Sang, Luqian Wang, Ying Yu, Jane J Lu, Taiying |
| description | Esophageal squamous cell carcinoma (ESCC) is the second common cancer in Henan province and is well-known for aggressiveness and dismal prognosis. Adjuvant therapies, chemotherapy, radiotherapy and endoscopic treatment have not improved survival rates in patients with late stage esophageal carcinoma. All-trans retinoic acid (ATRA) is the active ingredient of Vitamin A and affects a wide spectrum of biological processes including development, growth, neural function, immune function, reproduction, and vision. It is one of the most potent therapeutic agents used for treating cancers, especially lung adenocarcinomas. ATRA inhibits metastatic potential and angiogenesis in several tumor models. We investigated the effects of ATRA on the expression of angiopoietin 1 (Ang-1), angiopoietin 2 (Ang-2) and receptor Tie-2 in EC1 cells in vitro. We also assessed the growth and migration of EC1 cells in vitro. ATRA treatment caused 29.5% and 40.3% reduction of the growth of EC1 cells after 24 hours and 48 hours, relative to the control. ATRA plus fluorouracil treatment reduced the viability more strongly than either drug alone, indicating an additive effect. Moreover, ATRA decreased EC1 migration by 87%. Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Importantly, the protein levels of Ang-1, Ang-2 and Tie-2 were reduced by ATRA treatment. In vivo, we found ATRA treatment suppressed the tumor growth and improved the cachexia of mice. Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Collectively, our findings demonstrate that ATRA exhibits a dose- and temporal-dependent effect on the metastatic behavior, suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and the progression of xenograft tumors of EC1 cells. |
| doi_str_mv | 10.1371/journal.pone.0174555 |
| format | Article |
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Adjuvant therapies, chemotherapy, radiotherapy and endoscopic treatment have not improved survival rates in patients with late stage esophageal carcinoma. All-trans retinoic acid (ATRA) is the active ingredient of Vitamin A and affects a wide spectrum of biological processes including development, growth, neural function, immune function, reproduction, and vision. It is one of the most potent therapeutic agents used for treating cancers, especially lung adenocarcinomas. ATRA inhibits metastatic potential and angiogenesis in several tumor models. We investigated the effects of ATRA on the expression of angiopoietin 1 (Ang-1), angiopoietin 2 (Ang-2) and receptor Tie-2 in EC1 cells in vitro. We also assessed the growth and migration of EC1 cells in vitro. ATRA treatment caused 29.5% and 40.3% reduction of the growth of EC1 cells after 24 hours and 48 hours, relative to the control. ATRA plus fluorouracil treatment reduced the viability more strongly than either drug alone, indicating an additive effect. Moreover, ATRA decreased EC1 migration by 87%. Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Importantly, the protein levels of Ang-1, Ang-2 and Tie-2 were reduced by ATRA treatment. In vivo, we found ATRA treatment suppressed the tumor growth and improved the cachexia of mice. Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Collectively, our findings demonstrate that ATRA exhibits a dose- and temporal-dependent effect on the metastatic behavior, suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and the progression of xenograft tumors of EC1 cells.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0174555</identifier><identifier>PMID: 28369068</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>5-Fluorouracil ; Acids ; Adjuvant chemotherapy ; Analysis ; Angiogenesis ; Angiopoietin ; Angiopoietin-1 - biosynthesis ; Animal models ; Animals ; Antineoplastic Agents - pharmacology ; Apoptosis ; Biological activity ; Biology and Life Sciences ; Cachexia ; Cancer therapies ; Carcinoma, Squamous Cell - drug therapy ; Care and treatment ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cellular biology ; Chemical compounds ; Chemotherapy ; Diagnosis ; Esophageal cancer ; Esophageal carcinoma ; Esophageal Neoplasms - drug therapy ; Esophageal Squamous Cell Carcinoma ; Esophagus ; Female ; Fluorouracil - pharmacology ; Gene expression ; Health aspects ; Humans ; Immune response ; In vitro methods and tests ; Lung cancer ; Lungs ; Medicine and Health Sciences ; Metastases ; Metastasis ; Mice ; Mice, Inbred BALB C ; Neoplasm Metastasis - drug therapy ; Neovascularization, Pathologic - drug therapy ; Pharmacology ; Physical Sciences ; Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis ; Polymerase chain reaction ; Prognosis ; Radiation therapy ; Radiotherapy ; Receptor, TIE-2 - biosynthesis ; Receptors ; Receptors, Vascular Endothelial Growth Factor - biosynthesis ; Reproduction (biology) ; Retinoic acid ; Squamous cell carcinoma ; Survival ; Transcription ; Tretinoin ; Tretinoin - pharmacology ; Tumors ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - biosynthesis ; Vesicular Transport Proteins - biosynthesis ; Viability ; Vitamin A ; Xenografts</subject><ispartof>PloS one, 2017-04, Vol.12 (4), p.e0174555</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Li et al 2017 Li et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-ec8ab0c84c4742bf45ae57ac97ae7c49ffee186a5f95a3e319d10d0c270a6e3e3</citedby><cites>FETCH-LOGICAL-c758t-ec8ab0c84c4742bf45ae57ac97ae7c49ffee186a5f95a3e319d10d0c270a6e3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5378352/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5378352/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28369068$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Na</creatorcontrib><creatorcontrib>Lu, Yanjuan</creatorcontrib><creatorcontrib>Li, Daoming</creatorcontrib><creatorcontrib>Zheng, Xiangyu</creatorcontrib><creatorcontrib>Lian, Jingyao</creatorcontrib><creatorcontrib>Li, Shanshan</creatorcontrib><creatorcontrib>Cui, Huijuan</creatorcontrib><creatorcontrib>Zhang, Linda</creatorcontrib><creatorcontrib>Sang, Luqian</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Yu, Jane J</creatorcontrib><creatorcontrib>Lu, Taiying</creatorcontrib><title>All-trans retinoic acid suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and metastasis in esophageal squamous cell carcinoma</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Esophageal squamous cell carcinoma (ESCC) is the second common cancer in Henan province and is well-known for aggressiveness and dismal prognosis. Adjuvant therapies, chemotherapy, radiotherapy and endoscopic treatment have not improved survival rates in patients with late stage esophageal carcinoma. All-trans retinoic acid (ATRA) is the active ingredient of Vitamin A and affects a wide spectrum of biological processes including development, growth, neural function, immune function, reproduction, and vision. It is one of the most potent therapeutic agents used for treating cancers, especially lung adenocarcinomas. ATRA inhibits metastatic potential and angiogenesis in several tumor models. We investigated the effects of ATRA on the expression of angiopoietin 1 (Ang-1), angiopoietin 2 (Ang-2) and receptor Tie-2 in EC1 cells in vitro. We also assessed the growth and migration of EC1 cells in vitro. ATRA treatment caused 29.5% and 40.3% reduction of the growth of EC1 cells after 24 hours and 48 hours, relative to the control. ATRA plus fluorouracil treatment reduced the viability more strongly than either drug alone, indicating an additive effect. Moreover, ATRA decreased EC1 migration by 87%. Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Importantly, the protein levels of Ang-1, Ang-2 and Tie-2 were reduced by ATRA treatment. In vivo, we found ATRA treatment suppressed the tumor growth and improved the cachexia of mice. Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Collectively, our findings demonstrate that ATRA exhibits a dose- and temporal-dependent effect on the metastatic behavior, suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and the progression of xenograft tumors of EC1 cells.</description><subject>5-Fluorouracil</subject><subject>Acids</subject><subject>Adjuvant chemotherapy</subject><subject>Analysis</subject><subject>Angiogenesis</subject><subject>Angiopoietin</subject><subject>Angiopoietin-1 - biosynthesis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Biological activity</subject><subject>Biology and Life Sciences</subject><subject>Cachexia</subject><subject>Cancer therapies</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Care and treatment</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cellular biology</subject><subject>Chemical compounds</subject><subject>Chemotherapy</subject><subject>Diagnosis</subject><subject>Esophageal cancer</subject><subject>Esophageal carcinoma</subject><subject>Esophageal Neoplasms - drug therapy</subject><subject>Esophageal Squamous Cell Carcinoma</subject><subject>Esophagus</subject><subject>Female</subject><subject>Fluorouracil - pharmacology</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immune response</subject><subject>In vitro methods and tests</subject><subject>Lung cancer</subject><subject>Lungs</subject><subject>Medicine and Health Sciences</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Neoplasm Metastasis - drug therapy</subject><subject>Neovascularization, Pathologic - drug therapy</subject><subject>Pharmacology</subject><subject>Physical Sciences</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis</subject><subject>Polymerase chain reaction</subject><subject>Prognosis</subject><subject>Radiation therapy</subject><subject>Radiotherapy</subject><subject>Receptor, TIE-2 - biosynthesis</subject><subject>Receptors</subject><subject>Receptors, Vascular Endothelial Growth Factor - biosynthesis</subject><subject>Reproduction (biology)</subject><subject>Retinoic acid</subject><subject>Squamous cell carcinoma</subject><subject>Survival</subject><subject>Transcription</subject><subject>Tretinoin</subject><subject>Tretinoin - pharmacology</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - biosynthesis</subject><subject>Vesicular Transport Proteins - biosynthesis</subject><subject>Viability</subject><subject>Vitamin A</subject><subject>Xenografts</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk22L1DAQx4so3nn6DUQLguCLrulDmvTNwXL4sHBwoKdvw2w6bbO0Ta-Tqvcp_Mpmb3vHFhQkhaQzv_kn_JkJgpcxW8WpiN_v7DT20K4G2-OKxSLjnD8KTuMiTaI8Yenjo_NJ8IxoxxhPZZ4_DU4SmeYFy-Vp8HvdtpEboadwRGd6a3QI2pQhTcMwIhFS6BoMoa-NHazZM9G1wSQcwDU_4dZnytD0jdkaRwesxh7J0F2mQwfkP_9r-hDJDg3UCG1INxN0dqJQY9uGGkbtL-_gefCkgpbwxbyfBd8-fri--BxdXn3aXKwvIy24dBFqCVumZaYzkSXbKuOAXIAuBKDQWVFViLHMgVcFhxTTuChjVjKdCAY5-sBZ8PqgO7SW1OwlqVhKb5EUjHlicyBKCzs1jKaD8VZZMOouYMdaweiMblGBYDwWPJFcYlZshSxT729eskygzhPutc7n26Zth6XG3lveLkSXmd40qrY_FE-FTHniBd7MAqO9mZDcP548UzX4V5m-sl5Md4a0WmceY1la7LVWf6H8KrEz2ndTZXx8UfBuUeAZh79cDROR2nz98v_s1fcl-_aIbXxXuIZsOzlje1qC2QHUoyUasXpwLmZqPwz3bqj9MKh5GHzZq2PXH4ruuz_9A5CrCAA</recordid><startdate>20170403</startdate><enddate>20170403</enddate><creator>Li, Na</creator><creator>Lu, Yanjuan</creator><creator>Li, Daoming</creator><creator>Zheng, Xiangyu</creator><creator>Lian, Jingyao</creator><creator>Li, Shanshan</creator><creator>Cui, Huijuan</creator><creator>Zhang, Linda</creator><creator>Sang, Luqian</creator><creator>Wang, Ying</creator><creator>Yu, Jane J</creator><creator>Lu, Taiying</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20170403</creationdate><title>All-trans retinoic acid suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and metastasis in esophageal squamous cell carcinoma</title><author>Li, Na ; Lu, Yanjuan ; Li, Daoming ; Zheng, Xiangyu ; Lian, Jingyao ; Li, Shanshan ; Cui, Huijuan ; Zhang, Linda ; Sang, Luqian ; Wang, Ying ; Yu, Jane J ; Lu, Taiying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-ec8ab0c84c4742bf45ae57ac97ae7c49ffee186a5f95a3e319d10d0c270a6e3e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>5-Fluorouracil</topic><topic>Acids</topic><topic>Adjuvant chemotherapy</topic><topic>Analysis</topic><topic>Angiogenesis</topic><topic>Angiopoietin</topic><topic>Angiopoietin-1 - biosynthesis</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Biological activity</topic><topic>Biology and Life Sciences</topic><topic>Cachexia</topic><topic>Cancer therapies</topic><topic>Carcinoma, Squamous Cell - drug therapy</topic><topic>Care and treatment</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cellular biology</topic><topic>Chemical compounds</topic><topic>Chemotherapy</topic><topic>Diagnosis</topic><topic>Esophageal cancer</topic><topic>Esophageal carcinoma</topic><topic>Esophageal Neoplasms - drug therapy</topic><topic>Esophageal Squamous Cell Carcinoma</topic><topic>Esophagus</topic><topic>Female</topic><topic>Fluorouracil - pharmacology</topic><topic>Gene expression</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Immune response</topic><topic>In vitro methods and tests</topic><topic>Lung cancer</topic><topic>Lungs</topic><topic>Medicine and Health Sciences</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Neoplasm Metastasis - drug therapy</topic><topic>Neovascularization, Pathologic - drug therapy</topic><topic>Pharmacology</topic><topic>Physical Sciences</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis</topic><topic>Polymerase chain reaction</topic><topic>Prognosis</topic><topic>Radiation therapy</topic><topic>Radiotherapy</topic><topic>Receptor, TIE-2 - biosynthesis</topic><topic>Receptors</topic><topic>Receptors, Vascular Endothelial Growth Factor - biosynthesis</topic><topic>Reproduction (biology)</topic><topic>Retinoic acid</topic><topic>Squamous cell carcinoma</topic><topic>Survival</topic><topic>Transcription</topic><topic>Tretinoin</topic><topic>Tretinoin - pharmacology</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - biosynthesis</topic><topic>Vesicular Transport Proteins - biosynthesis</topic><topic>Viability</topic><topic>Vitamin A</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Na</creatorcontrib><creatorcontrib>Lu, Yanjuan</creatorcontrib><creatorcontrib>Li, Daoming</creatorcontrib><creatorcontrib>Zheng, Xiangyu</creatorcontrib><creatorcontrib>Lian, Jingyao</creatorcontrib><creatorcontrib>Li, Shanshan</creatorcontrib><creatorcontrib>Cui, Huijuan</creatorcontrib><creatorcontrib>Zhang, Linda</creatorcontrib><creatorcontrib>Sang, Luqian</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Yu, Jane J</creatorcontrib><creatorcontrib>Lu, Taiying</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Opposing Viewpoints Resource Center</collection><collection>Science (Gale in Context)</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Database (1962 - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>Biological Sciences</collection><collection>Agriculture Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>ProQuest Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content 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>Engineering collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Na</au><au>Lu, Yanjuan</au><au>Li, Daoming</au><au>Zheng, Xiangyu</au><au>Lian, Jingyao</au><au>Li, Shanshan</au><au>Cui, Huijuan</au><au>Zhang, Linda</au><au>Sang, Luqian</au><au>Wang, Ying</au><au>Yu, Jane J</au><au>Lu, Taiying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>All-trans retinoic acid suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and metastasis in esophageal squamous cell carcinoma</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-04-03</date><risdate>2017</risdate><volume>12</volume><issue>4</issue><spage>e0174555</spage><pages>e0174555-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Esophageal squamous cell carcinoma (ESCC) is the second common cancer in Henan province and is well-known for aggressiveness and dismal prognosis. Adjuvant therapies, chemotherapy, radiotherapy and endoscopic treatment have not improved survival rates in patients with late stage esophageal carcinoma. All-trans retinoic acid (ATRA) is the active ingredient of Vitamin A and affects a wide spectrum of biological processes including development, growth, neural function, immune function, reproduction, and vision. It is one of the most potent therapeutic agents used for treating cancers, especially lung adenocarcinomas. ATRA inhibits metastatic potential and angiogenesis in several tumor models. We investigated the effects of ATRA on the expression of angiopoietin 1 (Ang-1), angiopoietin 2 (Ang-2) and receptor Tie-2 in EC1 cells in vitro. We also assessed the growth and migration of EC1 cells in vitro. ATRA treatment caused 29.5% and 40.3% reduction of the growth of EC1 cells after 24 hours and 48 hours, relative to the control. ATRA plus fluorouracil treatment reduced the viability more strongly than either drug alone, indicating an additive effect. Moreover, ATRA decreased EC1 migration by 87%. Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Importantly, the protein levels of Ang-1, Ang-2 and Tie-2 were reduced by ATRA treatment. In vivo, we found ATRA treatment suppressed the tumor growth and improved the cachexia of mice. Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Collectively, our findings demonstrate that ATRA exhibits a dose- and temporal-dependent effect on the metastatic behavior, suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and the progression of xenograft tumors of EC1 cells.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28369068</pmid><doi>10.1371/journal.pone.0174555</doi><tpages>e0174555</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-04, Vol.12 (4), p.e0174555 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1883868700 |
| source | PubMed (Medline); MEDLINE; Public Library of Science; DOAJ Directory of Open Access Journals; Free Full-Text Journals in Chemistry; EZB Electronic Journals Library |
| subjects | 5-Fluorouracil Acids Adjuvant chemotherapy Analysis Angiogenesis Angiopoietin Angiopoietin-1 - biosynthesis Animal models Animals Antineoplastic Agents - pharmacology Apoptosis Biological activity Biology and Life Sciences Cachexia Cancer therapies Carcinoma, Squamous Cell - drug therapy Care and treatment Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Cellular biology Chemical compounds Chemotherapy Diagnosis Esophageal cancer Esophageal carcinoma Esophageal Neoplasms - drug therapy Esophageal Squamous Cell Carcinoma Esophagus Female Fluorouracil - pharmacology Gene expression Health aspects Humans Immune response In vitro methods and tests Lung cancer Lungs Medicine and Health Sciences Metastases Metastasis Mice Mice, Inbred BALB C Neoplasm Metastasis - drug therapy Neovascularization, Pathologic - drug therapy Pharmacology Physical Sciences Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis Polymerase chain reaction Prognosis Radiation therapy Radiotherapy Receptor, TIE-2 - biosynthesis Receptors Receptors, Vascular Endothelial Growth Factor - biosynthesis Reproduction (biology) Retinoic acid Squamous cell carcinoma Survival Transcription Tretinoin Tretinoin - pharmacology Tumors Vascular endothelial growth factor Vascular Endothelial Growth Factor A - biosynthesis Vesicular Transport Proteins - biosynthesis Viability Vitamin A Xenografts |
| title | All-trans retinoic acid suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and metastasis in esophageal squamous cell carcinoma |
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