Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR.
Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR.
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DOI：
10.1016/j.semcancer.2017.05.002
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发表时间：
2017-12
影响因子：
14.5
通讯作者：
Haynes CM
中科院分区：
文献类型：
--
作者：
Deng P;Haynes CM
线粒体形成细胞器或细胞隔室的细胞网络，其以ATP的形式有效地将营养素与能量产生偶联。由于癌细胞严重依赖糖酵解，因此历史上线粒体和维持线粒体活性的细胞途径被认为与肌肉和神经元等非分裂细胞中观察到的疾病更相关。然而，最近已经清楚的是，癌症严重依赖于线粒体活性，包括脂质、核苷酸和氨基酸合成，抑制线粒体介导的细胞凋亡以及氧化磷酸化（OXPHOS）以促进生长和存活。考虑到癌细胞线粒体可能引起的各种条件和压力，如缺氧，活性氧和线粒体基因组诱变，我们研究了被称为线粒体未折叠蛋白反应（UPRmt）的肿瘤保护性转录反应在癌细胞生物学中的潜在作用。
Mitochondria form a cellular network of organelles, or cellular compartments, that efficiently couple nutrients to energy production in the form of ATP. As cancer cells rely heavily on glycolysis, historically mitochondria and the cellular pathways in place to maintain mitochondrial activities were thought to be more relevant to diseases observed in non-dividing cells such as muscles and neurons. However, more recently it has become clear that cancers rely heavily on mitochondrial activities including lipid, nucleotide and amino acid synthesis, suppression of mitochondria-mediated apoptosis as well as oxidative phosphorylation (OXPHOS) for growth and survival. Considering the variety of conditions and stresses that cancer cell mitochondria may incur such as hypoxia, reactive oxygen species and mitochondrial genome mutagenesis, we examine potential roles for a mitochondrial-protective transcriptional response known as the mitochondrial unfolded protein response (UPRmt) in cancer cell biology.
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影响因子：
7.3
作者：
Gao J;Aksoy BA;Dogrusoz U;Dresdner G;Gross B;Sumer SO;Sun Y;Jacobsen A;Sinha R;Larsson E;Cerami E;Sander C;Schultz N
通讯作者：
Schultz N
影响因子：
6.4
作者：
Dasgupta, Santanu;Hoque, Mohammad Obaidul;Upadhyay, Sunil;Sidransky, David
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Sidransky, David
影响因子：
20.1
作者：
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影响因子：
2.1
作者：
Castilla, Carolina;Congregado, Belen;Saez, Carmen
通讯作者：
Saez, Carmen
影响因子：
7.4
作者：
Cano, Marisol;Wang, Lei;Wan, Jun;Barnett, Bradley P.;Ebrahimi, Katayoon;Qian, Jiang;Handa, James T.
通讯作者：
Handa, James T.