The gene encoding β-catenin is frequently mutated in hepatocellular carcinoma cells. While the oncogenicity of β-catenin has been extensively studied, β-catenin’s role in hepatocellular carcinoma tumor metabolism is currently less well understood...
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https://www.riss.kr/link?id=A106057182
2018
English
KCI등재,SCOPUS,SCIE
학술저널
1-7(7쪽)
3
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
The gene encoding β-catenin is frequently mutated in hepatocellular carcinoma cells. While the oncogenicity of β-catenin has been extensively studied, β-catenin’s role in hepatocellular carcinoma tumor metabolism is currently less well understood...
The gene encoding β-catenin is frequently mutated in hepatocellular carcinoma cells. While the oncogenicity of β-catenin has been extensively studied, β-catenin’s role in hepatocellular carcinoma tumor metabolism is currently less well understood. In this study, we found that β-catenin regulates the expression of glutamine synthetase and triggers a series of metabolic changes leading to induction of autophagy in hepatocellular carcinoma cells. β-Catenin-active Hep3B and HepG2 cells exhibited higher basal levels of autophagic activity than did β-catenin wild-type cells. We also found that autophagy in β-catenin-active cells was mediated by glutamine synthetase, as silencing of glutamine synthetase significantly reduced autophagic activity. We also showed that β-catenin-active hepatocellular carcinoma cells were more sensitive to sorafenib than were β-catenin wild-type cells.
Our results demonstrated that glutamine synthetase-mediated autophagy explains the high sensitivity of β-catenin-active hepatocellular carcinoma cells to sorafenib. Our results highlight the importance of glutamine metabolism in the regulation of autophagy in hepatocellular carcinoma cells. More importantly, our study unravels the molecular mechanisms leading to sorafenib sensitivity in hepatocellular carcinoma.
참고문헌 (Reference)
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1 Jungermann K, "Zonation of parenchymal and nonparenchymal metabolism in liver" 16 : 179-203, 1996
2 Shi YH, "Targeting autophagy enhances sorafenib lethality for hepatocellular carcinoma via ER stressrelated apoptosis" 7 : 1159-1172, 2011
3 Llovet JM, "Sorafenib in advanced hepatocellular carcinoma" 359 : 378-390, 2008
4 de La Coste A, "Somatic mutations of the beta-catenin gene are frequent in mouse and human hepatocellular carcinomas" 95 : 8847-8851, 1998
5 Marino G, "Self-consumption:the interplay of autophagy and apoptosis" 15 : 81-94, 2014
6 El-Serag HB, "Rising incidence of hepatocellular carcinoma in the United States" 340 : 745-750, 1999
7 Mosmann T, "Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays" 65 : 55-63, 1983
8 Hakvoort TB, "Pivotal role of glutamine synthetase in ammonia detoxification" 65 : 281-293, 2017
9 Minguez B, "Pathogenesis of hepatocellular carcinoma and molecular therapies" 25 : 186-194, 2009
10 Elgendy M, "Oncogenic Ras-induced expression of Noxa and Beclin-1 promotes autophagic cell death and limits clonogenic survival" 42 : 23-35, 2011
11 Cadoret A, "New targets of beta-catenin signaling in the liver are involved in the glutamine metabolism" 21 : 8293-8301, 2002
12 van der Vos KE, "Modulation of glutamine metabolism by the PI(3)K-PKB-FOXO network regulates autophagy" 14 : 829-837, 2012
13 Prieto-Dominguez N, "Modulation of autophagy by sorafenib: effects on treatment response" 7 : 151-, 2016
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Suppression of the ERK–SRF axis facilitates somatic cell reprogramming
Poly(rC) binding protein 2 acts as a negative regulator of IRES-mediated translation of Hr mRNA
학술지 이력
연월일 | 이력구분 | 이력상세 | 등재구분 |
---|---|---|---|
2023 | 평가예정 | 해외DB학술지평가 신청대상 (해외등재 학술지 평가) | |
2020-01-01 | 평가 | 등재학술지 유지 (해외등재 학술지 평가) | |
2009-09-21 | 학회명변경 | 한글명 : 대한생화학ㆍ분자생물학회 -> 생화학분자생물학회영문명 : Korean Society Of Medical Biochemistry And Molecular Biology -> Korean Society Of Biochemistry And Molecular Biology | |
2008-01-01 | 평가 | SCI 등재 (등재유지) | |
2006-01-01 | 평가 | 등재학술지 유지 (등재유지) | |
2004-01-01 | 평가 | 등재학술지 유지 (등재유지) | |
2001-01-01 | 평가 | 등재학술지 선정 (등재후보2차) | |
1998-07-01 | 평가 | 등재후보학술지 선정 (신규평가) |
학술지 인용정보
기준연도 | WOS-KCI 통합IF(2년) | KCIF(2년) | KCIF(3년) |
---|---|---|---|
2016 | 3.74 | 0.23 | 2.56 |
KCIF(4년) | KCIF(5년) | 중심성지수(3년) | 즉시성지수 |
1.82 | 1.45 | 0.555 | 0.01 |