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 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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source_id 49
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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imprint American Association for Cancer Research (AACR), 2018
imprint_str_mv American Association for Cancer Research (AACR), 2018
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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