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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Published in:OncoTargets and therapy 2018-01, Vol.11, p.5315
Main Authors: Yang, Chenggang, Li, Chaobin, Li, Shuangjing, Yang, Daogui, Du, Wenfeng, Liu, Xin
Format: Article
Language:English
Subjects:
Cancer
Colon cancer
Colorectal cancer
Comparative analysis
Drug resistance
EDTA
Fluorouracil
Health aspects
Molecular biology
Polymerase chain reaction
Proteins
RNA
Translation (Genetics)
Tumors
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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>314,780,784</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. 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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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source Publicly Available Content Database; Taylor & Francis Open Access Journals; 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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