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
Hauptverfasser: Yang, Chenggang, Li, Chaobin, Li, Shuangjing, Yang, Daogui, Du, Wenfeng, Liu, Xin
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container_start_page 5315
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creator Yang, Chenggang
Li, Chaobin
Li, Shuangjing
Yang, Daogui
Du, Wenfeng
Liu, Xin
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. 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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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