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Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway
Esophageal squamous cell carcinoma is the most common type of squamous cell carcinoma. Grape seed proanthocyanidin extract (GSPE) is considered to exhibit anticancer activity against several different types of cancer. We aimed to determine whether GSPE inhibited esophageal squamous cancerous cells a...
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Published in: | Mediators of inflammation 2018-01, Vol.2018 (2018), p.1-12 |
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description | Esophageal squamous cell carcinoma is the most common type of squamous cell carcinoma. Grape seed proanthocyanidin extract (GSPE) is considered to exhibit anticancer activity against several different types of cancer. We aimed to determine whether GSPE inhibited esophageal squamous cancerous cells and the possible involvement of NF-κB in this process. The human esophageal squamous cancer cell line ECA109 was treated with GSPE (0–80 μg/mL) and BAY11-7082 (10 μmol/L) for 12, 24, and 48 h. The MTT assay was used to determine cell proliferation; alterations in cell apoptosis were detected by flow cytometry; levels of inflammatory factors interleukin-6 and cyclooxygenase-2 and apoptotic proteins Bax/Bcl-2 were measured by ELISA; qRT-PCR and western blots were used to examine the activation of caspase-3 and NF-κB signaling. GSPE inhibited the proliferation of ECA109 cells and induced cellular apoptosis in a time- and dose-dependent manner. ELISA results showed that GSPE and BAY11-7082 reduced the secretion of inflammatory cytokines interleukin-6 and cyclooxygenase-2. The results of PCR and western blotting indicated that GSPE and BAY11-7082 activated caspase-3 and attenuated the activation of the NF-κB signaling pathway. GSPE induced apoptosis in ECA109 cells and inhibited ECA109 cell proliferation via a reduction in the secretion of inflammatory cytokines. This mechanism may be related to the attenuation of NF-κB activity and the sensitization of caspase-3. |
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Grape seed proanthocyanidin extract (GSPE) is considered to exhibit anticancer activity against several different types of cancer. We aimed to determine whether GSPE inhibited esophageal squamous cancerous cells and the possible involvement of NF-κB in this process. The human esophageal squamous cancer cell line ECA109 was treated with GSPE (0–80 μg/mL) and BAY11-7082 (10 μmol/L) for 12, 24, and 48 h. The MTT assay was used to determine cell proliferation; alterations in cell apoptosis were detected by flow cytometry; levels of inflammatory factors interleukin-6 and cyclooxygenase-2 and apoptotic proteins Bax/Bcl-2 were measured by ELISA; qRT-PCR and western blots were used to examine the activation of caspase-3 and NF-κB signaling. GSPE inhibited the proliferation of ECA109 cells and induced cellular apoptosis in a time- and dose-dependent manner. ELISA results showed that GSPE and BAY11-7082 reduced the secretion of inflammatory cytokines interleukin-6 and cyclooxygenase-2. The results of PCR and western blotting indicated that GSPE and BAY11-7082 activated caspase-3 and attenuated the activation of the NF-κB signaling pathway. GSPE induced apoptosis in ECA109 cells and inhibited ECA109 cell proliferation via a reduction in the secretion of inflammatory cytokines. This mechanism may be related to the attenuation of NF-κB activity and the sensitization of caspase-3.</description><identifier>ISSN: 0962-9351</identifier><identifier>EISSN: 1466-1861</identifier><identifier>DOI: 10.1155/2018/3403972</identifier><identifier>PMID: 30647533</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antitumor activity ; Apoptosis ; Apoptosis - drug effects ; Bax protein ; Bcl-2 protein ; Caspase ; Caspase 3 - metabolism ; Caspase-3 ; Cell adhesion & migration ; Cell culture ; Cell growth ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cyclooxygenase-2 ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Esophageal cancer ; Esophageal Neoplasms - metabolism ; Esophageal Squamous Cell Carcinoma - metabolism ; Esophagus ; Flow cytometry ; Free radicals ; Grape Seed Extract - pharmacology ; Humans ; Immunoglobulins ; Inflammation ; Interleukin 6 ; Liver cancer ; Medical prognosis ; Metastasis ; NF-kappa B - metabolism ; NF-κB protein ; Oncology ; Penicillin ; Proanthocyanidins - pharmacology ; Signal transduction ; Signal Transduction - drug effects ; Squamous cell carcinoma ; Western blotting</subject><ispartof>Mediators of inflammation, 2018-01, Vol.2018 (2018), p.1-12</ispartof><rights>Copyright © 2018 Fangming Guo et al.</rights><rights>Copyright © 2018 Fangming Guo et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Fangming Guo et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c537t-ac001e4aad5c3b2c792f8324be5e87c513ce3196e5fb65b7cc3b891026b6eb9c3</citedby><cites>FETCH-LOGICAL-c537t-ac001e4aad5c3b2c792f8324be5e87c513ce3196e5fb65b7cc3b891026b6eb9c3</cites><orcidid>0000-0002-0789-0005 ; 0000-0001-7972-0470 ; 0000-0002-9278-6412</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2161643978/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2161643978?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30647533$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Terrazas, Luis I.</contributor><contributor>Luis I Terrazas</contributor><creatorcontrib>Xie, Jianxin</creatorcontrib><creatorcontrib>Li, Shugang</creatorcontrib><creatorcontrib>Ma, Ru-Lin</creatorcontrib><creatorcontrib>Ding, Yu-Song</creatorcontrib><creatorcontrib>Li, Yu</creatorcontrib><creatorcontrib>Niu, Qiang</creatorcontrib><creatorcontrib>Hu, Yun-Hua</creatorcontrib><creatorcontrib>Guo, Fangming</creatorcontrib><creatorcontrib>Wang, Xianhua</creatorcontrib><title>Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway</title><title>Mediators of inflammation</title><addtitle>Mediators Inflamm</addtitle><description>Esophageal squamous cell carcinoma is the most common type of squamous cell carcinoma. Grape seed proanthocyanidin extract (GSPE) is considered to exhibit anticancer activity against several different types of cancer. We aimed to determine whether GSPE inhibited esophageal squamous cancerous cells and the possible involvement of NF-κB in this process. The human esophageal squamous cancer cell line ECA109 was treated with GSPE (0–80 μg/mL) and BAY11-7082 (10 μmol/L) for 12, 24, and 48 h. The MTT assay was used to determine cell proliferation; alterations in cell apoptosis were detected by flow cytometry; levels of inflammatory factors interleukin-6 and cyclooxygenase-2 and apoptotic proteins Bax/Bcl-2 were measured by ELISA; qRT-PCR and western blots were used to examine the activation of caspase-3 and NF-κB signaling. GSPE inhibited the proliferation of ECA109 cells and induced cellular apoptosis in a time- and dose-dependent manner. ELISA results showed that GSPE and BAY11-7082 reduced the secretion of inflammatory cytokines interleukin-6 and cyclooxygenase-2. The results of PCR and western blotting indicated that GSPE and BAY11-7082 activated caspase-3 and attenuated the activation of the NF-κB signaling pathway. GSPE induced apoptosis in ECA109 cells and inhibited ECA109 cell proliferation via a reduction in the secretion of inflammatory cytokines. This mechanism may be related to the attenuation of NF-κB activity and the sensitization of caspase-3.</description><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>Caspase</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell adhesion & migration</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cyclooxygenase-2</subject><subject>Cytokines</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - metabolism</subject><subject>Esophageal Squamous Cell Carcinoma - metabolism</subject><subject>Esophagus</subject><subject>Flow cytometry</subject><subject>Free radicals</subject><subject>Grape Seed Extract - pharmacology</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Oncology</subject><subject>Penicillin</subject><subject>Proanthocyanidins - pharmacology</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Squamous cell carcinoma</subject><subject>Western blotting</subject><issn>0962-9351</issn><issn>1466-1861</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNkk9v0zAYhyMEYmNw44wscUGCMP-JneSCNKpuq1TBpMLZeuO8aVylduckG73ysfgQfCbctQzGiZOt148e2T__kuQlo-8Zk_KUU1acioyKMuePkmOWKZWyQrHHyTEtFU9LIdlR8qzvV5RSmWXF0-RIUJXlUojj5PtFgA2SBWJNroIHN7TebMHZ2joy_TYEMAOZudZWdujJ5biGOO79poUlQkcW1yOs_diTCTiD4W6HXUfm1iGZTs4YLcmNBTK0SD6dpz9_fCQLu3TQWbckVzC0t7B9njxpoOvxxWE9Sb6eT79MLtP554vZ5GyeGinyIQVDKcMMoJZGVNzkJW8KwbMKJRa5kUwYFKxUKJtKySo3kSpKRrmqFFalESfJbO-tPaz0Jtg1hK32YPXdwIelhjBY06EGVDlK0fA6kxltioJGialMw5WiULLo-rB3bcZqjbVBF5PqHkgfnjjb6qW_0UowVkoZBW8OguCvR-wHvba9idGBw5ii5iwv448yxiP6-h905ccQM9xRiqksckWk3u0pE3zfB2zuL8Oo3hVF74qiD0WJ-Ku_H3AP_25GBN7ugda6Gm7tf-owMtjAH5pTIaUSvwARHtAJ</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Xie, Jianxin</creator><creator>Li, Shugang</creator><creator>Ma, Ru-Lin</creator><creator>Ding, Yu-Song</creator><creator>Li, Yu</creator><creator>Niu, Qiang</creator><creator>Hu, Yun-Hua</creator><creator>Guo, Fangming</creator><creator>Wang, Xianhua</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0789-0005</orcidid><orcidid>https://orcid.org/0000-0001-7972-0470</orcidid><orcidid>https://orcid.org/0000-0002-9278-6412</orcidid></search><sort><creationdate>20180101</creationdate><title>Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway</title><author>Xie, Jianxin ; Li, Shugang ; Ma, Ru-Lin ; Ding, Yu-Song ; Li, Yu ; Niu, Qiang ; Hu, Yun-Hua ; Guo, Fangming ; Wang, Xianhua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c537t-ac001e4aad5c3b2c792f8324be5e87c513ce3196e5fb65b7cc3b891026b6eb9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>Caspase</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Cell adhesion & migration</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cyclooxygenase-2</topic><topic>Cytokines</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Esophageal cancer</topic><topic>Esophageal Neoplasms - metabolism</topic><topic>Esophageal Squamous Cell Carcinoma - metabolism</topic><topic>Esophagus</topic><topic>Flow cytometry</topic><topic>Free radicals</topic><topic>Grape Seed Extract - pharmacology</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>NF-kappa B - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Mediators of inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Jianxin</au><au>Li, Shugang</au><au>Ma, Ru-Lin</au><au>Ding, Yu-Song</au><au>Li, Yu</au><au>Niu, Qiang</au><au>Hu, Yun-Hua</au><au>Guo, Fangming</au><au>Wang, Xianhua</au><au>Terrazas, Luis I.</au><au>Luis I Terrazas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway</atitle><jtitle>Mediators of inflammation</jtitle><addtitle>Mediators Inflamm</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>0962-9351</issn><eissn>1466-1861</eissn><abstract>Esophageal squamous cell carcinoma is the most common type of squamous cell carcinoma. Grape seed proanthocyanidin extract (GSPE) is considered to exhibit anticancer activity against several different types of cancer. We aimed to determine whether GSPE inhibited esophageal squamous cancerous cells and the possible involvement of NF-κB in this process. The human esophageal squamous cancer cell line ECA109 was treated with GSPE (0–80 μg/mL) and BAY11-7082 (10 μmol/L) for 12, 24, and 48 h. The MTT assay was used to determine cell proliferation; alterations in cell apoptosis were detected by flow cytometry; levels of inflammatory factors interleukin-6 and cyclooxygenase-2 and apoptotic proteins Bax/Bcl-2 were measured by ELISA; qRT-PCR and western blots were used to examine the activation of caspase-3 and NF-κB signaling. GSPE inhibited the proliferation of ECA109 cells and induced cellular apoptosis in a time- and dose-dependent manner. ELISA results showed that GSPE and BAY11-7082 reduced the secretion of inflammatory cytokines interleukin-6 and cyclooxygenase-2. The results of PCR and western blotting indicated that GSPE and BAY11-7082 activated caspase-3 and attenuated the activation of the NF-κB signaling pathway. GSPE induced apoptosis in ECA109 cells and inhibited ECA109 cell proliferation via a reduction in the secretion of inflammatory cytokines. This mechanism may be related to the attenuation of NF-κB activity and the sensitization of caspase-3.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30647533</pmid><doi>10.1155/2018/3403972</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0789-0005</orcidid><orcidid>https://orcid.org/0000-0001-7972-0470</orcidid><orcidid>https://orcid.org/0000-0002-9278-6412</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antitumor activity Apoptosis Apoptosis - drug effects Bax protein Bcl-2 protein Caspase Caspase 3 - metabolism Caspase-3 Cell adhesion & migration Cell culture Cell growth Cell Line, Tumor Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Cell Survival - drug effects Cyclooxygenase-2 Cytokines Enzyme-Linked Immunosorbent Assay Esophageal cancer Esophageal Neoplasms - metabolism Esophageal Squamous Cell Carcinoma - metabolism Esophagus Flow cytometry Free radicals Grape Seed Extract - pharmacology Humans Immunoglobulins Inflammation Interleukin 6 Liver cancer Medical prognosis Metastasis NF-kappa B - metabolism NF-κB protein Oncology Penicillin Proanthocyanidins - pharmacology Signal transduction Signal Transduction - drug effects Squamous cell carcinoma Western blotting |
title | Grape Seed Proanthocyanidin Extract Inhibits Human Esophageal Squamous Cancerous Cell Line ECA109 via the NF-κB Signaling Pathway |
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