Eukaryotic translation initiation factor 3 subunit G
Purpose: Colorectal cancer (CRC) has become a predominant cancer and accounts for approximately 10% of cancer-related mortality. Drug resistance still remains a priority mortality factor for patients due to no available therapeutic alternatives. The purpose of the present study was to investigate th...
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Veröffentlicht in: | OncoTargets and therapy 2018-01, Vol.11, p.5315 |
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description | Purpose: Colorectal cancer (CRC) has become a predominant cancer and accounts for approximately 10% of cancer-related mortality. Drug resistance still remains a priority mortality factor for patients due to no available therapeutic alternatives. The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Methods: Multiple cellular and molecular biology experiments were performed in the present study, such as CCK-8, western blotting and flow cytometry. Results: We found that EIF3G is highly expressed at RNA and protein levels in HCT116/5-Fu cells compared with HCT116 cells using quantitative real-time polymerase chain reaction and Western blot analysis. In addition, silencing EIF3G enhanced 5-Fu-induced apoptosis in HCT116/5-Fu cells. Moreover, EIF3G silencing decreased the activity of the drug-related proteins MDR1 and MRP levels in HCT116/5-Fu cells. Finally, the xenograft tumor model further confirmed that EIF3G resensitized HCT116/5-Fu tumors to 5-Fu. We observed that EIF3G silencing followed by 5-Fu administration had a synergistic interaction effect on HCT116/5-Fu in vitro and in vivo. Conclusion: These findings demonstrate that EIF3G is a targetable regulator of chemoresistance in CRC, and inhibiting EIF3G in combination with 5-Fu might be a potential therapeutic strategy for colon cancer. Keywords: EIF3G, colorectal cancer, 5-fluorouracil, drug resistance, MDR1, MRP |
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Drug resistance still remains a priority mortality factor for patients due to no available therapeutic alternatives. The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Methods: Multiple cellular and molecular biology experiments were performed in the present study, such as CCK-8, western blotting and flow cytometry. Results: We found that EIF3G is highly expressed at RNA and protein levels in HCT116/5-Fu cells compared with HCT116 cells using quantitative real-time polymerase chain reaction and Western blot analysis. In addition, silencing EIF3G enhanced 5-Fu-induced apoptosis in HCT116/5-Fu cells. Moreover, EIF3G silencing decreased the activity of the drug-related proteins MDR1 and MRP levels in HCT116/5-Fu cells. Finally, the xenograft tumor model further confirmed that EIF3G resensitized HCT116/5-Fu tumors to 5-Fu. We observed that EIF3G silencing followed by 5-Fu administration had a synergistic interaction effect on HCT116/5-Fu in vitro and in vivo. Conclusion: These findings demonstrate that EIF3G is a targetable regulator of chemoresistance in CRC, and inhibiting EIF3G in combination with 5-Fu might be a potential therapeutic strategy for colon cancer. Keywords: EIF3G, colorectal cancer, 5-fluorouracil, drug resistance, MDR1, MRP</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><language>eng</language><publisher>Dove Medical Press Limited</publisher><subject>Cancer ; Colon cancer ; Colorectal cancer ; Comparative analysis ; Drug resistance ; EDTA ; Fluorouracil ; Health aspects ; Molecular biology ; Polymerase chain reaction ; Proteins ; RNA ; Translation (Genetics) ; Tumors</subject><ispartof>OncoTargets and therapy, 2018-01, Vol.11, p.5315</ispartof><rights>COPYRIGHT 2018 Dove Medical Press Limited</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785</link.rule.ids></links><search><creatorcontrib>Yang, Chenggang</creatorcontrib><creatorcontrib>Li, Chaobin</creatorcontrib><creatorcontrib>Li, Shuangjing</creatorcontrib><creatorcontrib>Yang, Daogui</creatorcontrib><creatorcontrib>Du, Wenfeng</creatorcontrib><creatorcontrib>Liu, Xin</creatorcontrib><title>Eukaryotic translation initiation factor 3 subunit G</title><title>OncoTargets and therapy</title><description>Purpose: Colorectal cancer (CRC) has become a predominant cancer and accounts for approximately 10% of cancer-related mortality. Drug resistance still remains a priority mortality factor for patients due to no available therapeutic alternatives. The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Methods: Multiple cellular and molecular biology experiments were performed in the present study, such as CCK-8, western blotting and flow cytometry. Results: We found that EIF3G is highly expressed at RNA and protein levels in HCT116/5-Fu cells compared with HCT116 cells using quantitative real-time polymerase chain reaction and Western blot analysis. In addition, silencing EIF3G enhanced 5-Fu-induced apoptosis in HCT116/5-Fu cells. Moreover, EIF3G silencing decreased the activity of the drug-related proteins MDR1 and MRP levels in HCT116/5-Fu cells. Finally, the xenograft tumor model further confirmed that EIF3G resensitized HCT116/5-Fu tumors to 5-Fu. We observed that EIF3G silencing followed by 5-Fu administration had a synergistic interaction effect on HCT116/5-Fu in vitro and in vivo. Conclusion: These findings demonstrate that EIF3G is a targetable regulator of chemoresistance in CRC, and inhibiting EIF3G in combination with 5-Fu might be a potential therapeutic strategy for colon cancer. Keywords: EIF3G, colorectal cancer, 5-fluorouracil, drug resistance, MDR1, MRP</description><subject>Cancer</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Comparative analysis</subject><subject>Drug resistance</subject><subject>EDTA</subject><subject>Fluorouracil</subject><subject>Health aspects</subject><subject>Molecular biology</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>RNA</subject><subject>Translation (Genetics)</subject><subject>Tumors</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNpjYuA0NDS30DWzNDZgQWJzMHAVF2cZGJiZWRiZcDKYuJZmJxZV5pdkJiuUFCXmFecklmTm5ylk5mWWZEKYaYnJJflFCsYKxaVJpUBhBXceBta0xJziVF4ozc2g5uYa4uyhm56YkxqfkZqYU5JRnJ9TCtJeHO9oamFsZmliaWZoTLRCAMkxOH0</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Yang, Chenggang</creator><creator>Li, Chaobin</creator><creator>Li, Shuangjing</creator><creator>Yang, Daogui</creator><creator>Du, Wenfeng</creator><creator>Liu, Xin</creator><general>Dove Medical Press Limited</general><scope/></search><sort><creationdate>20180101</creationdate><title>Eukaryotic translation initiation factor 3 subunit G</title><author>Yang, Chenggang ; Li, Chaobin ; Li, Shuangjing ; Yang, Daogui ; Du, Wenfeng ; Liu, Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-gale_healthsolutions_A5836949613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Cancer</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Comparative analysis</topic><topic>Drug resistance</topic><topic>EDTA</topic><topic>Fluorouracil</topic><topic>Health aspects</topic><topic>Molecular biology</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>RNA</topic><topic>Translation (Genetics)</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Chenggang</creatorcontrib><creatorcontrib>Li, Chaobin</creatorcontrib><creatorcontrib>Li, Shuangjing</creatorcontrib><creatorcontrib>Yang, Daogui</creatorcontrib><creatorcontrib>Du, Wenfeng</creatorcontrib><creatorcontrib>Liu, Xin</creatorcontrib><jtitle>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Chenggang</au><au>Li, Chaobin</au><au>Li, Shuangjing</au><au>Yang, Daogui</au><au>Du, Wenfeng</au><au>Liu, Xin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Eukaryotic translation initiation factor 3 subunit G</atitle><jtitle>OncoTargets and therapy</jtitle><date>2018-01-01</date><risdate>2018</risdate><volume>11</volume><spage>5315</spage><pages>5315-</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>Purpose: Colorectal cancer (CRC) has become a predominant cancer and accounts for approximately 10% of cancer-related mortality. Drug resistance still remains a priority mortality factor for patients due to no available therapeutic alternatives. The purpose of the present study was to investigate the underlying molecular mechanisms how eukaryotic translation initiation factor 3 subunit G (EIF3G) resensitized 5-Fu-resistant human CRC cells (HCT116/5-Fu) to 5-fluorouracil (5-Fu). Methods: Multiple cellular and molecular biology experiments were performed in the present study, such as CCK-8, western blotting and flow cytometry. Results: We found that EIF3G is highly expressed at RNA and protein levels in HCT116/5-Fu cells compared with HCT116 cells using quantitative real-time polymerase chain reaction and Western blot analysis. In addition, silencing EIF3G enhanced 5-Fu-induced apoptosis in HCT116/5-Fu cells. Moreover, EIF3G silencing decreased the activity of the drug-related proteins MDR1 and MRP levels in HCT116/5-Fu cells. Finally, the xenograft tumor model further confirmed that EIF3G resensitized HCT116/5-Fu tumors to 5-Fu. We observed that EIF3G silencing followed by 5-Fu administration had a synergistic interaction effect on HCT116/5-Fu in vitro and in vivo. Conclusion: These findings demonstrate that EIF3G is a targetable regulator of chemoresistance in CRC, and inhibiting EIF3G in combination with 5-Fu might be a potential therapeutic strategy for colon cancer. Keywords: EIF3G, colorectal cancer, 5-fluorouracil, drug resistance, MDR1, MRP</abstract><pub>Dove Medical Press Limited</pub></addata></record> |
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source | Dove Press Free; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Access via Taylor & Francis (Open Access Collection); PubMed Central |
subjects | Cancer Colon cancer Colorectal cancer Comparative analysis Drug resistance EDTA Fluorouracil Health aspects Molecular biology Polymerase chain reaction Proteins RNA Translation (Genetics) Tumors |
title | Eukaryotic translation initiation factor 3 subunit G |
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