ADAM17-siRNA inhibits MCF-7 breast cancer through EGFR-PI3K-AKT activation
A disintegrin and metalloproteinase-17 (ADAM17) can cut and release a wide variety of epidermal growth factor receptor (EGFR) ligands to promote survival, invasion and proliferation of cancer cell, and therefore, is considered to be a potential therapeutic target for cancer. The main goal of the pre...
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| Veröffentlicht in: | International journal of oncology 2016-08, Vol.49 (2), p.682-690 |
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| creator | Meng, Xiangchao Hu, Baoshan Hossain, Mohammad Monir Chen, Guofu Sun, Ying Zhang, Xuepeng |
| description | A disintegrin and metalloproteinase-17 (ADAM17) can cut and release a wide variety of epidermal growth factor receptor (EGFR) ligands to promote survival, invasion and proliferation of cancer cell, and therefore, is considered to be a potential therapeutic target for cancer. The main goal of the present study was to observe the effects of ADAM17 small interfering RNA (ADAM17-siRNA) on human MCF-7 breast cancer and investigate its activation pathway. In vitro, MCF-7 cells were divided into ADAM17-siRNA groups, nonsense siRNA groups, AG1478 (selective EGFR blocker) groups, LY294002 [phosphatidylinositol 3-kinase (PI3K) phosphorylation inhibitor] groups, PD0325901 [mitogen extracellular kinase (MEK) inhibitor] groups and control groups. In vivo, MCF-7 cells were implanted subcutaneously into nude mice and then these mice were randomly divided into ADAM17-siRNA groups, vector groups and control groups. Our data showed that compared with the control groups, ADAM17-siRNA, AG1478 and LY294002 could inhibit the migration and proliferation of MCF-7 cells, but PD0325901 and nonsense siRNA did not show this effect. Except that specific ADAM17-siRNA could inhibit the expression of ADAM17 mRNA, others did not change it. Western blot analysis further confirmed that EGFR-PI3K-AKT signaling pathway is involved in ADAM17-siRNA inhibiting migration and proliferation of MCF-7 cells. Similarly to the former, the growth of MCF-7 breast cancer in nude mice was significantly inhibited by ADAM17-siRNA. Compared with the control group and the vector group, the tumor volume was smaller in the ADAM17-siRNA group, the tissues developed large areas of necrosis, immunohistochemistry showed low expressions of ADAM17 and Ki-67 and western blot analysis proved that the expression of ADAM17 protein in the tissue was also reduced. The present study suggests that ADAM17-siRNA inhibits MCF-7 breast cancer and is activated through the EGFR-PI3K-AKT signaling pathway. |
| doi_str_mv | 10.3892/ijo.2016.3536 |
| format | Article |
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The main goal of the present study was to observe the effects of ADAM17 small interfering RNA (ADAM17-siRNA) on human MCF-7 breast cancer and investigate its activation pathway. In vitro, MCF-7 cells were divided into ADAM17-siRNA groups, nonsense siRNA groups, AG1478 (selective EGFR blocker) groups, LY294002 [phosphatidylinositol 3-kinase (PI3K) phosphorylation inhibitor] groups, PD0325901 [mitogen extracellular kinase (MEK) inhibitor] groups and control groups. In vivo, MCF-7 cells were implanted subcutaneously into nude mice and then these mice were randomly divided into ADAM17-siRNA groups, vector groups and control groups. Our data showed that compared with the control groups, ADAM17-siRNA, AG1478 and LY294002 could inhibit the migration and proliferation of MCF-7 cells, but PD0325901 and nonsense siRNA did not show this effect. Except that specific ADAM17-siRNA could inhibit the expression of ADAM17 mRNA, others did not change it. Western blot analysis further confirmed that EGFR-PI3K-AKT signaling pathway is involved in ADAM17-siRNA inhibiting migration and proliferation of MCF-7 cells. Similarly to the former, the growth of MCF-7 breast cancer in nude mice was significantly inhibited by ADAM17-siRNA. Compared with the control group and the vector group, the tumor volume was smaller in the ADAM17-siRNA group, the tissues developed large areas of necrosis, immunohistochemistry showed low expressions of ADAM17 and Ki-67 and western blot analysis proved that the expression of ADAM17 protein in the tissue was also reduced. The present study suggests that ADAM17-siRNA inhibits MCF-7 breast cancer and is activated through the EGFR-PI3K-AKT signaling pathway.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2016.3536</identifier><identifier>PMID: 27221510</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject><![CDATA[a disintegrin and metalloprotease 17 ; ADAM17 Protein - antagonists & inhibitors ; ADAM17 Protein - genetics ; Animals ; Benzamides - administration & dosage ; Binding sites ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cell adhesion & migration ; Cell growth ; Cellular signal transduction ; Chromones - administration & dosage ; Development and progression ; Diphenylamine - administration & dosage ; Diphenylamine - analogs & derivatives ; EGFR-PI3K-AKT signaling pathway ; Enzymes ; Female ; Gene amplification ; Gene expression ; Genetic aspects ; Growth factors ; Health aspects ; Humans ; Kinases ; MCF-7 Cells ; Medical prognosis ; Metastasis ; Mice ; Morpholines - administration & dosage ; Phosphatidylinositol 3-Kinase - antagonists & inhibitors ; Phosphatidylinositol 3-Kinase - genetics ; Proteases ; Proteins ; Proto-Oncogene Proteins c-akt - antagonists & inhibitors ; Proto-Oncogene Proteins c-akt - genetics ; Quinazolines - administration & dosage ; Receptor, Epidermal Growth Factor - antagonists & inhibitors ; Receptor, Epidermal Growth Factor - genetics ; RNA, Small Interfering - genetics ; Signal Transduction - drug effects ; small interference RNA ; Studies ; targeted therapy ; Tumor necrosis factor-TNF ; Tumors ; Tyrphostins - administration & dosage ; Xenograft Model Antitumor Assays]]></subject><ispartof>International journal of oncology, 2016-08, Vol.49 (2), p.682-690</ispartof><rights>Copyright © 2016, Spandidos Publications</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c556t-78e3f332aedbd8d697ffa28828afa88e5456f4623cc2a4919b8b2648ef5268b93</citedby><cites>FETCH-LOGICAL-c556t-78e3f332aedbd8d697ffa28828afa88e5456f4623cc2a4919b8b2648ef5268b93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27221510$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meng, Xiangchao</creatorcontrib><creatorcontrib>Hu, Baoshan</creatorcontrib><creatorcontrib>Hossain, Mohammad Monir</creatorcontrib><creatorcontrib>Chen, Guofu</creatorcontrib><creatorcontrib>Sun, Ying</creatorcontrib><creatorcontrib>Zhang, Xuepeng</creatorcontrib><title>ADAM17-siRNA inhibits MCF-7 breast cancer through EGFR-PI3K-AKT activation</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>A disintegrin and metalloproteinase-17 (ADAM17) can cut and release a wide variety of epidermal growth factor receptor (EGFR) ligands to promote survival, invasion and proliferation of cancer cell, and therefore, is considered to be a potential therapeutic target for cancer. The main goal of the present study was to observe the effects of ADAM17 small interfering RNA (ADAM17-siRNA) on human MCF-7 breast cancer and investigate its activation pathway. In vitro, MCF-7 cells were divided into ADAM17-siRNA groups, nonsense siRNA groups, AG1478 (selective EGFR blocker) groups, LY294002 [phosphatidylinositol 3-kinase (PI3K) phosphorylation inhibitor] groups, PD0325901 [mitogen extracellular kinase (MEK) inhibitor] groups and control groups. In vivo, MCF-7 cells were implanted subcutaneously into nude mice and then these mice were randomly divided into ADAM17-siRNA groups, vector groups and control groups. Our data showed that compared with the control groups, ADAM17-siRNA, AG1478 and LY294002 could inhibit the migration and proliferation of MCF-7 cells, but PD0325901 and nonsense siRNA did not show this effect. Except that specific ADAM17-siRNA could inhibit the expression of ADAM17 mRNA, others did not change it. Western blot analysis further confirmed that EGFR-PI3K-AKT signaling pathway is involved in ADAM17-siRNA inhibiting migration and proliferation of MCF-7 cells. Similarly to the former, the growth of MCF-7 breast cancer in nude mice was significantly inhibited by ADAM17-siRNA. Compared with the control group and the vector group, the tumor volume was smaller in the ADAM17-siRNA group, the tissues developed large areas of necrosis, immunohistochemistry showed low expressions of ADAM17 and Ki-67 and western blot analysis proved that the expression of ADAM17 protein in the tissue was also reduced. The present study suggests that ADAM17-siRNA inhibits MCF-7 breast cancer and is activated through the EGFR-PI3K-AKT signaling pathway.</description><subject>a disintegrin and metalloprotease 17</subject><subject>ADAM17 Protein - antagonists & inhibitors</subject><subject>ADAM17 Protein - genetics</subject><subject>Animals</subject><subject>Benzamides - administration & dosage</subject><subject>Binding sites</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cellular signal transduction</subject><subject>Chromones - administration & dosage</subject><subject>Development and progression</subject><subject>Diphenylamine - administration & dosage</subject><subject>Diphenylamine - analogs & derivatives</subject><subject>EGFR-PI3K-AKT signaling pathway</subject><subject>Enzymes</subject><subject>Female</subject><subject>Gene amplification</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>MCF-7 Cells</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Morpholines - administration & dosage</subject><subject>Phosphatidylinositol 3-Kinase - antagonists & inhibitors</subject><subject>Phosphatidylinositol 3-Kinase - genetics</subject><subject>Proteases</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Quinazolines - administration & dosage</subject><subject>Receptor, Epidermal Growth Factor - antagonists & inhibitors</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>RNA, Small Interfering - genetics</subject><subject>Signal Transduction - drug effects</subject><subject>small interference RNA</subject><subject>Studies</subject><subject>targeted therapy</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumors</subject><subject>Tyrphostins - administration & dosage</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkcFvFCEUh4nR2Lp69GomMdETKzwGBo6TtVtrWzVNPROGgQ6b3WGFGRP_e9lsrTYxHCDke-_l_T6EXlOyZFLBh7CJSyBULBln4gk6pY2iGGpgT8ubUIVFzdQJepHzhhDgnNDn6AQaAMopOUWf24_tNW1wDjdf2iqMQ-jClKvr1Ro3VZecyVNlzWhdqqYhxfluqM7O1zf42wW7xO3lbWXsFH6aKcTxJXrmzTa7V_f3An1fn92uPuGrr-cXq_YKW87FhBvpmGcMjOu7XvZCNd4bkBKk8UZKx2sufC2AWQumVlR1sgNRS-c5CNkptkBvj333Kf6YXZ70Js5pLCM1VQwYiIaQv9Sd2TodRh-nZOwuZKvbmivBJSuJLdDyP1Q5vdsFG0fnQ_l_VPDun4LBme005LidDwHkxyA-gjbFnJPzep_CzqRfmhJ9MKeLOX0wpw_mCv_mfqu527n-gf6jqgDvj0Dem7EPfcwPTOmEa4UJYCIksN8hq5rN</recordid><startdate>20160801</startdate><enddate>20160801</enddate><creator>Meng, Xiangchao</creator><creator>Hu, Baoshan</creator><creator>Hossain, Mohammad Monir</creator><creator>Chen, Guofu</creator><creator>Sun, Ying</creator><creator>Zhang, Xuepeng</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20160801</creationdate><title>ADAM17-siRNA inhibits MCF-7 breast cancer through EGFR-PI3K-AKT activation</title><author>Meng, Xiangchao ; Hu, Baoshan ; Hossain, Mohammad Monir ; Chen, Guofu ; Sun, Ying ; Zhang, Xuepeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c556t-78e3f332aedbd8d697ffa28828afa88e5456f4623cc2a4919b8b2648ef5268b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>a disintegrin and metalloprotease 17</topic><topic>ADAM17 Protein - antagonists & inhibitors</topic><topic>ADAM17 Protein - genetics</topic><topic>Animals</topic><topic>Benzamides - administration & dosage</topic><topic>Binding sites</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cellular signal transduction</topic><topic>Chromones - administration & dosage</topic><topic>Development and progression</topic><topic>Diphenylamine - administration & dosage</topic><topic>Diphenylamine - analogs & derivatives</topic><topic>EGFR-PI3K-AKT signaling pathway</topic><topic>Enzymes</topic><topic>Female</topic><topic>Gene amplification</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>MCF-7 Cells</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Morpholines - administration & dosage</topic><topic>Phosphatidylinositol 3-Kinase - antagonists & inhibitors</topic><topic>Phosphatidylinositol 3-Kinase - genetics</topic><topic>Proteases</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Quinazolines - administration & dosage</topic><topic>Receptor, Epidermal Growth Factor - antagonists & inhibitors</topic><topic>Receptor, Epidermal Growth Factor - genetics</topic><topic>RNA, Small Interfering - genetics</topic><topic>Signal Transduction - drug effects</topic><topic>small interference RNA</topic><topic>Studies</topic><topic>targeted therapy</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumors</topic><topic>Tyrphostins - administration & dosage</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meng, Xiangchao</creatorcontrib><creatorcontrib>Hu, Baoshan</creatorcontrib><creatorcontrib>Hossain, Mohammad Monir</creatorcontrib><creatorcontrib>Chen, Guofu</creatorcontrib><creatorcontrib>Sun, Ying</creatorcontrib><creatorcontrib>Zhang, Xuepeng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meng, Xiangchao</au><au>Hu, Baoshan</au><au>Hossain, Mohammad Monir</au><au>Chen, Guofu</au><au>Sun, Ying</au><au>Zhang, Xuepeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ADAM17-siRNA inhibits MCF-7 breast cancer through EGFR-PI3K-AKT activation</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2016-08-01</date><risdate>2016</risdate><volume>49</volume><issue>2</issue><spage>682</spage><epage>690</epage><pages>682-690</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>A disintegrin and metalloproteinase-17 (ADAM17) can cut and release a wide variety of epidermal growth factor receptor (EGFR) ligands to promote survival, invasion and proliferation of cancer cell, and therefore, is considered to be a potential therapeutic target for cancer. The main goal of the present study was to observe the effects of ADAM17 small interfering RNA (ADAM17-siRNA) on human MCF-7 breast cancer and investigate its activation pathway. In vitro, MCF-7 cells were divided into ADAM17-siRNA groups, nonsense siRNA groups, AG1478 (selective EGFR blocker) groups, LY294002 [phosphatidylinositol 3-kinase (PI3K) phosphorylation inhibitor] groups, PD0325901 [mitogen extracellular kinase (MEK) inhibitor] groups and control groups. In vivo, MCF-7 cells were implanted subcutaneously into nude mice and then these mice were randomly divided into ADAM17-siRNA groups, vector groups and control groups. Our data showed that compared with the control groups, ADAM17-siRNA, AG1478 and LY294002 could inhibit the migration and proliferation of MCF-7 cells, but PD0325901 and nonsense siRNA did not show this effect. Except that specific ADAM17-siRNA could inhibit the expression of ADAM17 mRNA, others did not change it. Western blot analysis further confirmed that EGFR-PI3K-AKT signaling pathway is involved in ADAM17-siRNA inhibiting migration and proliferation of MCF-7 cells. Similarly to the former, the growth of MCF-7 breast cancer in nude mice was significantly inhibited by ADAM17-siRNA. Compared with the control group and the vector group, the tumor volume was smaller in the ADAM17-siRNA group, the tissues developed large areas of necrosis, immunohistochemistry showed low expressions of ADAM17 and Ki-67 and western blot analysis proved that the expression of ADAM17 protein in the tissue was also reduced. The present study suggests that ADAM17-siRNA inhibits MCF-7 breast cancer and is activated through the EGFR-PI3K-AKT signaling pathway.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>27221510</pmid><doi>10.3892/ijo.2016.3536</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | a disintegrin and metalloprotease 17 ADAM17 Protein - antagonists & inhibitors ADAM17 Protein - genetics Animals Benzamides - administration & dosage Binding sites Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - pathology Cell adhesion & migration Cell growth Cellular signal transduction Chromones - administration & dosage Development and progression Diphenylamine - administration & dosage Diphenylamine - analogs & derivatives EGFR-PI3K-AKT signaling pathway Enzymes Female Gene amplification Gene expression Genetic aspects Growth factors Health aspects Humans Kinases MCF-7 Cells Medical prognosis Metastasis Mice Morpholines - administration & dosage Phosphatidylinositol 3-Kinase - antagonists & inhibitors Phosphatidylinositol 3-Kinase - genetics Proteases Proteins Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - genetics Quinazolines - administration & dosage Receptor, Epidermal Growth Factor - antagonists & inhibitors Receptor, Epidermal Growth Factor - genetics RNA, Small Interfering - genetics Signal Transduction - drug effects small interference RNA Studies targeted therapy Tumor necrosis factor-TNF Tumors Tyrphostins - administration & dosage Xenograft Model Antitumor Assays |
| title | ADAM17-siRNA inhibits MCF-7 breast cancer through EGFR-PI3K-AKT activation |
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