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Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch
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Zeitschriftentitel: | Cancer Research |
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Personen und Körperschaften: | , , , , , , , , , , , , , , , |
In: | Cancer Research, 78, 2018, 11, S. 2813-2824 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
American Association for Cancer Research (AACR)
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Schlagwörter: |
author_facet |
Zhu, Ping Liu, Yongzhang Zhang, Fenglin Bai, Xiufeng Chen, Zilei Shangguan, Fugen Zhang, Bo Zhang, Lingyun Chen, Qianqian Xie, Deyao Lan, Linhua Xue, Xiangdong Liang, Xing-Jie Lu, Bin Wei, Taotao Qin, Yan Zhu, Ping Liu, Yongzhang Zhang, Fenglin Bai, Xiufeng Chen, Zilei Shangguan, Fugen Zhang, Bo Zhang, Lingyun Chen, Qianqian Xie, Deyao Lan, Linhua Xue, Xiangdong Liang, Xing-Jie Lu, Bin Wei, Taotao Qin, Yan |
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author |
Zhu, Ping Liu, Yongzhang Zhang, Fenglin Bai, Xiufeng Chen, Zilei Shangguan, Fugen Zhang, Bo Zhang, Lingyun Chen, Qianqian Xie, Deyao Lan, Linhua Xue, Xiangdong Liang, Xing-Jie Lu, Bin Wei, Taotao Qin, Yan |
spellingShingle |
Zhu, Ping Liu, Yongzhang Zhang, Fenglin Bai, Xiufeng Chen, Zilei Shangguan, Fugen Zhang, Bo Zhang, Lingyun Chen, Qianqian Xie, Deyao Lan, Linhua Xue, Xiangdong Liang, Xing-Jie Lu, Bin Wei, Taotao Qin, Yan Cancer Research Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch Cancer Research Oncology |
author_sort |
zhu, ping |
spelling |
Zhu, Ping Liu, Yongzhang Zhang, Fenglin Bai, Xiufeng Chen, Zilei Shangguan, Fugen Zhang, Bo Zhang, Lingyun Chen, Qianqian Xie, Deyao Lan, Linhua Xue, Xiangdong Liang, Xing-Jie Lu, Bin Wei, Taotao Qin, Yan 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-17-2059 <jats:title>Abstract</jats:title> <jats:p>Mitochondria regulate cellular bioenergetics and redox states and influence multiple signaling pathways required for tumorigenesis. In this study, we determined that the mitochondrial translation elongation factor 4 (EF4) is a critical component of tumor progression. EF4 was ubiquitous in human tissues with localization to the mitochondria (mtEF4) and performed quality control on respiratory chain biogenesis. Knockout of mtEF4 induced respiratory chain complex defects and apoptosis, while its overexpression stimulated cancer development. In multiple cancers, expression of mtEF4 was increased in patient tumor tissues. These findings reveal that mtEF4 expression may promote tumorigenesis via an imbalance in the regulation of mitochondrial activities and subsequent variation of cellular redox. Thus, dysregulated mitochondrial translation may play a vital role in the etiology and development of diverse human cancers.</jats:p> <jats:p>Significance: Dysregulated mitochondrial translation drives tumor development and progression. Cancer Res; 78(11); 2813–24. ©2018 AACR.</jats:p> Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch Cancer Research |
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10.1158/0008-5472.can-17-2059 |
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American Association for Cancer Research (AACR), 2018 |
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American Association for Cancer Research (AACR), 2018 |
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0008-5472 1538-7445 |
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Cancer Research |
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title |
Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_unstemmed |
Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_full |
Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_fullStr |
Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_full_unstemmed |
Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_short |
Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_sort |
human elongation factor 4 regulates cancer bioenergetics by acting as a mitochondrial translation switch |
topic |
Cancer Research Oncology |
url |
http://dx.doi.org/10.1158/0008-5472.can-17-2059 |
publishDate |
2018 |
physical |
2813-2824 |
description |
<jats:title>Abstract</jats:title>
<jats:p>Mitochondria regulate cellular bioenergetics and redox states and influence multiple signaling pathways required for tumorigenesis. In this study, we determined that the mitochondrial translation elongation factor 4 (EF4) is a critical component of tumor progression. EF4 was ubiquitous in human tissues with localization to the mitochondria (mtEF4) and performed quality control on respiratory chain biogenesis. Knockout of mtEF4 induced respiratory chain complex defects and apoptosis, while its overexpression stimulated cancer development. In multiple cancers, expression of mtEF4 was increased in patient tumor tissues. These findings reveal that mtEF4 expression may promote tumorigenesis via an imbalance in the regulation of mitochondrial activities and subsequent variation of cellular redox. Thus, dysregulated mitochondrial translation may play a vital role in the etiology and development of diverse human cancers.</jats:p>
<jats:p>Significance: Dysregulated mitochondrial translation drives tumor development and progression. Cancer Res; 78(11); 2813–24. ©2018 AACR.</jats:p> |
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author | Zhu, Ping, Liu, Yongzhang, Zhang, Fenglin, Bai, Xiufeng, Chen, Zilei, Shangguan, Fugen, Zhang, Bo, Zhang, Lingyun, Chen, Qianqian, Xie, Deyao, Lan, Linhua, Xue, Xiangdong, Liang, Xing-Jie, Lu, Bin, Wei, Taotao, Qin, Yan |
author_facet | Zhu, Ping, Liu, Yongzhang, Zhang, Fenglin, Bai, Xiufeng, Chen, Zilei, Shangguan, Fugen, Zhang, Bo, Zhang, Lingyun, Chen, Qianqian, Xie, Deyao, Lan, Linhua, Xue, Xiangdong, Liang, Xing-Jie, Lu, Bin, Wei, Taotao, Qin, Yan, Zhu, Ping, Liu, Yongzhang, Zhang, Fenglin, Bai, Xiufeng, Chen, Zilei, Shangguan, Fugen, Zhang, Bo, Zhang, Lingyun, Chen, Qianqian, Xie, Deyao, Lan, Linhua, Xue, Xiangdong, Liang, Xing-Jie, Lu, Bin, Wei, Taotao, Qin, Yan |
author_sort | zhu, ping |
container_issue | 11 |
container_start_page | 2813 |
container_title | Cancer Research |
container_volume | 78 |
description | <jats:title>Abstract</jats:title> <jats:p>Mitochondria regulate cellular bioenergetics and redox states and influence multiple signaling pathways required for tumorigenesis. In this study, we determined that the mitochondrial translation elongation factor 4 (EF4) is a critical component of tumor progression. EF4 was ubiquitous in human tissues with localization to the mitochondria (mtEF4) and performed quality control on respiratory chain biogenesis. Knockout of mtEF4 induced respiratory chain complex defects and apoptosis, while its overexpression stimulated cancer development. In multiple cancers, expression of mtEF4 was increased in patient tumor tissues. These findings reveal that mtEF4 expression may promote tumorigenesis via an imbalance in the regulation of mitochondrial activities and subsequent variation of cellular redox. Thus, dysregulated mitochondrial translation may play a vital role in the etiology and development of diverse human cancers.</jats:p> <jats:p>Significance: Dysregulated mitochondrial translation drives tumor development and progression. Cancer Res; 78(11); 2813–24. ©2018 AACR.</jats:p> |
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spelling | Zhu, Ping Liu, Yongzhang Zhang, Fenglin Bai, Xiufeng Chen, Zilei Shangguan, Fugen Zhang, Bo Zhang, Lingyun Chen, Qianqian Xie, Deyao Lan, Linhua Xue, Xiangdong Liang, Xing-Jie Lu, Bin Wei, Taotao Qin, Yan 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-17-2059 <jats:title>Abstract</jats:title> <jats:p>Mitochondria regulate cellular bioenergetics and redox states and influence multiple signaling pathways required for tumorigenesis. In this study, we determined that the mitochondrial translation elongation factor 4 (EF4) is a critical component of tumor progression. EF4 was ubiquitous in human tissues with localization to the mitochondria (mtEF4) and performed quality control on respiratory chain biogenesis. Knockout of mtEF4 induced respiratory chain complex defects and apoptosis, while its overexpression stimulated cancer development. In multiple cancers, expression of mtEF4 was increased in patient tumor tissues. These findings reveal that mtEF4 expression may promote tumorigenesis via an imbalance in the regulation of mitochondrial activities and subsequent variation of cellular redox. Thus, dysregulated mitochondrial translation may play a vital role in the etiology and development of diverse human cancers.</jats:p> <jats:p>Significance: Dysregulated mitochondrial translation drives tumor development and progression. Cancer Res; 78(11); 2813–24. ©2018 AACR.</jats:p> Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch Cancer Research |
spellingShingle | Zhu, Ping, Liu, Yongzhang, Zhang, Fenglin, Bai, Xiufeng, Chen, Zilei, Shangguan, Fugen, Zhang, Bo, Zhang, Lingyun, Chen, Qianqian, Xie, Deyao, Lan, Linhua, Xue, Xiangdong, Liang, Xing-Jie, Lu, Bin, Wei, Taotao, Qin, Yan, Cancer Research, Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch, Cancer Research, Oncology |
title | Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_full | Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_fullStr | Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_full_unstemmed | Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_short | Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
title_sort | human elongation factor 4 regulates cancer bioenergetics by acting as a mitochondrial translation switch |
title_unstemmed | Human Elongation Factor 4 Regulates Cancer Bioenergetics by Acting as a Mitochondrial Translation Switch |
topic | Cancer Research, Oncology |
url | http://dx.doi.org/10.1158/0008-5472.can-17-2059 |