Role and mechanism of action of LRIG1 in ovarian cancer cell line and VP16 drug-resistant cell line
We investigated the role of leucine-rich repeats and immunoglobulin-like domains (LRIG)-1 in ovarian cancer cell line and VP16 drug-resistant cell line to explore the possible mechanism of action. Human ovarian cancer cell line SKOV3 and the VP16 drug-resistant cell line SKOV3/VP16 were used to inve...
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| Veröffentlicht in: | Oncology letters 2017-10, Vol.14 (4), p.4619-4624 |
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| creator | Zhang, Yaqi Liu, Zhizhen Yu, Shunrui |
| description | We investigated the role of leucine-rich repeats and immunoglobulin-like domains (LRIG)-1 in ovarian cancer cell line and VP16 drug-resistant cell line to explore the possible mechanism of action. Human ovarian cancer cell line SKOV3 and the VP16 drug-resistant cell line SKOV3/VP16 were used to investigate whether LRIG1 affects the sensitivity of SKOV3 to drugs. RT-qPCR was used to detect the difference in LRIG1 expression between drug-resistant and wild-type cell lines. siRNA LRIG1 was designed and transfected to silence LRIG1 to investigate the mechanism by which LRIG1 affects the sensitivity of SKOV3 to drugs. Wild-type cells were transfected with SKOV3. The cells were divided into 3 groups (VP16, NC + VP16 and siRNA LRIG1 + VP16 treatment group). VP16 (IC
value) was added 24 h after transfection. The CCK-8 method was used to detect the proliferation of each group at multiple time points (0, 24, 48 and 72 h). A colony-forming assay was used to detect cell proliferation and flow cytometry was used to detect cell apoptosis. The expression of LRIG1 was lower in the drug resistant cell line than that of the wild-type cell line. The expression of LRIG1 significantly decreased with the increase of VP16 concentration (P |
| doi_str_mv | 10.3892/ol.2017.6730 |
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value) was added 24 h after transfection. The CCK-8 method was used to detect the proliferation of each group at multiple time points (0, 24, 48 and 72 h). A colony-forming assay was used to detect cell proliferation and flow cytometry was used to detect cell apoptosis. The expression of LRIG1 was lower in the drug resistant cell line than that of the wild-type cell line. The expression of LRIG1 significantly decreased with the increase of VP16 concentration (P<0.05). The apoptotic rate was decreased but there was an increase on cell clones in the siLRIG1 + VP16-treated group as compared to VP16- and NC+ VP16-treated groups (P<0.05). The
gene affects the sensitivity of SKOV3 cells to drug in a dose-related manner, indicating that the reduced expression of LRIG1 can inhibit cell apoptosis.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2017.6730</identifier><identifier>PMID: 28943962</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Alcohol ; Apoptosis ; Cancer therapies ; Cell cycle ; Cell division ; Cell growth ; Cervical cancer ; Deoxyribonucleic acid ; DNA ; Drug dosages ; Drug resistance ; Enzymes ; Growth factors ; Kinases ; Oncology ; Ovarian cancer ; Standard deviation ; Tumors</subject><ispartof>Oncology letters, 2017-10, Vol.14 (4), p.4619-4624</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Zhang et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-138df682581d2eb9a31324d1784a8dea87b4480dada4b80301ba37e3b616bf053</citedby><cites>FETCH-LOGICAL-c412t-138df682581d2eb9a31324d1784a8dea87b4480dada4b80301ba37e3b616bf053</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/PMC5592861/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5592861/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28943962$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yaqi</creatorcontrib><creatorcontrib>Liu, Zhizhen</creatorcontrib><creatorcontrib>Yu, Shunrui</creatorcontrib><title>Role and mechanism of action of LRIG1 in ovarian cancer cell line and VP16 drug-resistant cell line</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>We investigated the role of leucine-rich repeats and immunoglobulin-like domains (LRIG)-1 in ovarian cancer cell line and VP16 drug-resistant cell line to explore the possible mechanism of action. Human ovarian cancer cell line SKOV3 and the VP16 drug-resistant cell line SKOV3/VP16 were used to investigate whether LRIG1 affects the sensitivity of SKOV3 to drugs. RT-qPCR was used to detect the difference in LRIG1 expression between drug-resistant and wild-type cell lines. siRNA LRIG1 was designed and transfected to silence LRIG1 to investigate the mechanism by which LRIG1 affects the sensitivity of SKOV3 to drugs. Wild-type cells were transfected with SKOV3. The cells were divided into 3 groups (VP16, NC + VP16 and siRNA LRIG1 + VP16 treatment group). VP16 (IC
value) was added 24 h after transfection. The CCK-8 method was used to detect the proliferation of each group at multiple time points (0, 24, 48 and 72 h). A colony-forming assay was used to detect cell proliferation and flow cytometry was used to detect cell apoptosis. The expression of LRIG1 was lower in the drug resistant cell line than that of the wild-type cell line. The expression of LRIG1 significantly decreased with the increase of VP16 concentration (P<0.05). The apoptotic rate was decreased but there was an increase on cell clones in the siLRIG1 + VP16-treated group as compared to VP16- and NC+ VP16-treated groups (P<0.05). The
gene affects the sensitivity of SKOV3 cells to drug in a dose-related manner, indicating that the reduced expression of LRIG1 can inhibit cell apoptosis.</description><subject>Alcohol</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Cervical cancer</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Drug dosages</subject><subject>Drug resistance</subject><subject>Enzymes</subject><subject>Growth factors</subject><subject>Kinases</subject><subject>Oncology</subject><subject>Ovarian cancer</subject><subject>Standard deviation</subject><subject>Tumors</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkc1rFTEUxYNYbKnduZaAGxedZ26SycdGkFJr4YGlqNuQSTJtykxSk5lC__vO8Oqrejc5kN893MNB6B2QDVOafsrDhhKQGyEZeYWOQGraAFH09V5LfohOar0jy7QClBJv0CFVmjMt6BFy13kI2CaPx-BubYp1xLnH1k0xp1Vtry8vAMdFP9gSbcLOJhcKdmEY8BDTbvnXFQjsy3zTlFBjnWyaXoi36KC3Qw0nz-8x-vn1_MfZt2b7_eLy7Mu2cRzo1ABTvheKtgo8DZ22DBjlHqTiVvlglew4V8Rbb3mnCCPQWSYD6wSIrictO0afd773czcG70Kaih3MfYmjLY8m22j-_Unx1tzkB9O2mioBi8HHZ4OSf8-hTmaMdY1hU8hzNaA5lcCEFAv64T_0Ls8lLfEWSmqgVBO1UKc7ypVcawn9_hggZi3Q5MGsBZq1wAV__3eAPfynLvYE8JaU2A</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Zhang, Yaqi</creator><creator>Liu, Zhizhen</creator><creator>Yu, Shunrui</creator><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</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>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171001</creationdate><title>Role and mechanism of action of LRIG1 in ovarian cancer cell line and VP16 drug-resistant cell line</title><author>Zhang, Yaqi ; Liu, Zhizhen ; Yu, Shunrui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-138df682581d2eb9a31324d1784a8dea87b4480dada4b80301ba37e3b616bf053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Alcohol</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Cervical cancer</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Drug dosages</topic><topic>Drug resistance</topic><topic>Enzymes</topic><topic>Growth factors</topic><topic>Kinases</topic><topic>Oncology</topic><topic>Ovarian cancer</topic><topic>Standard deviation</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yaqi</creatorcontrib><creatorcontrib>Liu, Zhizhen</creatorcontrib><creatorcontrib>Yu, Shunrui</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>Health & Medical Collection (Alumni Edition)</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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yaqi</au><au>Liu, Zhizhen</au><au>Yu, Shunrui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role and mechanism of action of LRIG1 in ovarian cancer cell line and VP16 drug-resistant cell line</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>14</volume><issue>4</issue><spage>4619</spage><epage>4624</epage><pages>4619-4624</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>We investigated the role of leucine-rich repeats and immunoglobulin-like domains (LRIG)-1 in ovarian cancer cell line and VP16 drug-resistant cell line to explore the possible mechanism of action. Human ovarian cancer cell line SKOV3 and the VP16 drug-resistant cell line SKOV3/VP16 were used to investigate whether LRIG1 affects the sensitivity of SKOV3 to drugs. RT-qPCR was used to detect the difference in LRIG1 expression between drug-resistant and wild-type cell lines. siRNA LRIG1 was designed and transfected to silence LRIG1 to investigate the mechanism by which LRIG1 affects the sensitivity of SKOV3 to drugs. Wild-type cells were transfected with SKOV3. The cells were divided into 3 groups (VP16, NC + VP16 and siRNA LRIG1 + VP16 treatment group). VP16 (IC
value) was added 24 h after transfection. The CCK-8 method was used to detect the proliferation of each group at multiple time points (0, 24, 48 and 72 h). A colony-forming assay was used to detect cell proliferation and flow cytometry was used to detect cell apoptosis. The expression of LRIG1 was lower in the drug resistant cell line than that of the wild-type cell line. The expression of LRIG1 significantly decreased with the increase of VP16 concentration (P<0.05). The apoptotic rate was decreased but there was an increase on cell clones in the siLRIG1 + VP16-treated group as compared to VP16- and NC+ VP16-treated groups (P<0.05). The
gene affects the sensitivity of SKOV3 cells to drug in a dose-related manner, indicating that the reduced expression of LRIG1 can inhibit cell apoptosis.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>28943962</pmid><doi>10.3892/ol.2017.6730</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Alcohol Apoptosis Cancer therapies Cell cycle Cell division Cell growth Cervical cancer Deoxyribonucleic acid DNA Drug dosages Drug resistance Enzymes Growth factors Kinases Oncology Ovarian cancer Standard deviation Tumors |
| title | Role and mechanism of action of LRIG1 in ovarian cancer cell line and VP16 drug-resistant cell line |
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