Serveur d'exploration sur la glutarédoxine

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Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS.

Identifieur interne : 000458 ( Main/Exploration ); précédent : 000457; suivant : 000459

Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS.

Auteurs : Feng He [République populaire de Chine] ; Lili Wei [République populaire de Chine] ; Wenqi Luo [République populaire de Chine] ; Zhipeng Liao [République populaire de Chine] ; Bo Li [République populaire de Chine] ; Xiaoying Zhou [République populaire de Chine] ; Xue Xiao [République populaire de Chine] ; Jingping You [République populaire de Chine] ; Yufeng Chen [République populaire de Chine] ; Shixing Zheng [République populaire de Chine] ; Ping Li [République populaire de Chine] ; Mariko Murata [Japon] ; Guangwu Huang [République populaire de Chine] ; Zhe Zhang [République populaire de Chine]

Source :

RBID : pubmed:27203742

Descripteurs français

English descriptors

Abstract

Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was overexpressed in NPC. Knockdown of GLRX3 in NPC cell lines inhibited proliferation in vitro, tumorignesis in vivo, and colony formation. In addition, GLRX3 knockdown decreased the migration and invasion capacity of NPC cells by reversing the epithelial-mesenchymal transition (EMT). Furthermore, stabilization of GLRX3 was positively related to with epidermal growth factor receptor (EGFR) expression and negatively with ROS generation. Phosphorylation of Akt, a key downstream effector, was induced by EGFR signaling but did not rely on increasing ROS level in NPC cells. GLRX3 might be an oncoprotein in NPC, playing important roles in increasing redox reaction and activating EGFR/ Akt signals, so it may be a therapeutic target for NPC.

DOI: 10.18632/oncotarget.9454
PubMed: 27203742
PubMed Central: PMC5095054


Affiliations:


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Le document en format XML

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<term>Adult (MeSH)</term>
<term>Aged (MeSH)</term>
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<term>Tumeurs du rhinopharynx</term>
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<term>Signal Transduction</term>
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<term>Mice</term>
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<term>Middle Aged</term>
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<term>Reactive Oxygen Species</term>
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<term>Animaux</term>
<term>Cancer du nasopharynx</term>
<term>Espèces réactives de l'oxygène</term>
<term>Femelle</term>
<term>Humains</term>
<term>Hétérogreffes</term>
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<div type="abstract" xml:lang="en">Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was overexpressed in NPC. Knockdown of GLRX3 in NPC cell lines inhibited proliferation in vitro, tumorignesis in vivo, and colony formation. In addition, GLRX3 knockdown decreased the migration and invasion capacity of NPC cells by reversing the epithelial-mesenchymal transition (EMT). Furthermore, stabilization of GLRX3 was positively related to with epidermal growth factor receptor (EGFR) expression and negatively with ROS generation. Phosphorylation of Akt, a key downstream effector, was induced by EGFR signaling but did not rely on increasing ROS level in NPC cells. GLRX3 might be an oncoprotein in NPC, playing important roles in increasing redox reaction and activating EGFR/ Akt signals, so it may be a therapeutic target for NPC.</div>
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<Year>2018</Year>
<Month>01</Month>
<Day>12</Day>
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<Year>2019</Year>
<Month>02</Month>
<Day>21</Day>
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<ISSN IssnType="Electronic">1949-2553</ISSN>
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<Volume>7</Volume>
<Issue>24</Issue>
<PubDate>
<Year>2016</Year>
<Month>Jun</Month>
<Day>14</Day>
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<Title>Oncotarget</Title>
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<ArticleTitle>Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS.</ArticleTitle>
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<AbstractText>Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was overexpressed in NPC. Knockdown of GLRX3 in NPC cell lines inhibited proliferation in vitro, tumorignesis in vivo, and colony formation. In addition, GLRX3 knockdown decreased the migration and invasion capacity of NPC cells by reversing the epithelial-mesenchymal transition (EMT). Furthermore, stabilization of GLRX3 was positively related to with epidermal growth factor receptor (EGFR) expression and negatively with ROS generation. Phosphorylation of Akt, a key downstream effector, was induced by EGFR signaling but did not rely on increasing ROS level in NPC cells. GLRX3 might be an oncoprotein in NPC, playing important roles in increasing redox reaction and activating EGFR/ Akt signals, so it may be a therapeutic target for NPC.</AbstractText>
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<ForeName>Feng</ForeName>
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<Affiliation>Department of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning, China.</Affiliation>
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<name sortKey="Chen, Yufeng" sort="Chen, Yufeng" uniqKey="Chen Y" first="Yufeng" last="Chen">Yufeng Chen</name>
<name sortKey="Huang, Guangwu" sort="Huang, Guangwu" uniqKey="Huang G" first="Guangwu" last="Huang">Guangwu Huang</name>
<name sortKey="Li, Bo" sort="Li, Bo" uniqKey="Li B" first="Bo" last="Li">Bo Li</name>
<name sortKey="Li, Ping" sort="Li, Ping" uniqKey="Li P" first="Ping" last="Li">Ping Li</name>
<name sortKey="Liao, Zhipeng" sort="Liao, Zhipeng" uniqKey="Liao Z" first="Zhipeng" last="Liao">Zhipeng Liao</name>
<name sortKey="Luo, Wenqi" sort="Luo, Wenqi" uniqKey="Luo W" first="Wenqi" last="Luo">Wenqi Luo</name>
<name sortKey="Wei, Lili" sort="Wei, Lili" uniqKey="Wei L" first="Lili" last="Wei">Lili Wei</name>
<name sortKey="Xiao, Xue" sort="Xiao, Xue" uniqKey="Xiao X" first="Xue" last="Xiao">Xue Xiao</name>
<name sortKey="You, Jingping" sort="You, Jingping" uniqKey="You J" first="Jingping" last="You">Jingping You</name>
<name sortKey="Zhang, Zhe" sort="Zhang, Zhe" uniqKey="Zhang Z" first="Zhe" last="Zhang">Zhe Zhang</name>
<name sortKey="Zheng, Shixing" sort="Zheng, Shixing" uniqKey="Zheng S" first="Shixing" last="Zheng">Shixing Zheng</name>
<name sortKey="Zhou, Xiaoying" sort="Zhou, Xiaoying" uniqKey="Zhou X" first="Xiaoying" last="Zhou">Xiaoying Zhou</name>
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<country name="Japon">
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<name sortKey="Murata, Mariko" sort="Murata, Mariko" uniqKey="Murata M" first="Mariko" last="Murata">Mariko Murata</name>
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