Inhibition of epithelial cell migration and Src/FAK signaling by SIRT3

Lee, Jaewon J.; Ven, Robert A. H. van de; Zaganjor, Elma; Ng, Mei Rosa; Barakat, Amey; Demmers, Joris J. P. G.; Finley, Lydia W.S.; Herrera, Karina N. Gonzalez; Hung, Yin P.; Harris, Isaac S.; Jeong, Seung Min; Danuser, Gaudenz; McAllister, Sandra S.; Haigis, Marcia C.

doi:10.1073/pnas.1800440115

Cited by 57 publications

(40 citation statements)

References 38 publications

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“…Importantly, SIRT3 loss is heterozygous, suggesting selective pressure to maintain an intact copy of the gene ( Finley et al, 2011 ). When the prognostic value of individual UPR mt genes was analyzed, elevated SIRT3 was associated with better relapse-free survival ( Figure S3F ), in agreement with a recent report ( Lee et al, 2018 ). This observation is consistent with a study demonstrating that SIRT3 overexpression in MDA-MB-231 cells delays tumor growth in xenografts ( Gonzalez Herrera et al, 2018 ).…”

Section: Discussionsupporting

confidence: 90%

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Mitohormesis Primes Tumor Invasion and Metastasis

et al. 2019

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Section: Discussionsupporting

confidence: 90%

“…It is important to note that this overexpression far exceeds the endogenous levels found in invasive cells, such as MDA-MB-231. The same group also demonstrated that SIRT3 is downregulated in the invasive front of MCF10A cells ( Lee et al, 2018 ). To reconcile these observations, we propose the following model ( Figure S4 ).…”

Section: Discussionmentioning

confidence: 88%

Mitohormesis Primes Tumor Invasion and Metastasis

et al. 2019

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“…In addition, SIRT3 directly or indirectly inhibits ROS-regulated tumorigenesis and metastasis 90 . Of which, SIRT3 represses ROS dependent Src/FAK signaling and promotes the proliferation, migration and metastasis of cancer cells 91 . ROS elimination by SIRT3 was also proven to contribute to the growth inhibition of lung adenocarcinoma cells 92 .…”

Section: Sirt3 and Human Diseasementioning

confidence: 99%

Mitochondrial Sirtuin 3: New emerging biological function and therapeutic target

Zhang¹,

Xiang²,

Liu³

et al. 2020

Theranostics

246

238

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Sirtuin 3 (SIRT3) is one of the most prominent deacetylases that can regulate acetylation levels in mitochondria, which are essential for eukaryotic life and inextricably linked to the metabolism of multiple organs. Hitherto, SIRT3 has been substantiated to be involved in almost all aspects of mitochondrial metabolism and homeostasis, protecting mitochondria from a variety of damage. Accumulating evidence has recently documented that SIRT3 is associated with many types of human diseases, including age-related diseases, cancer, heart disease and metabolic diseases, indicating that SIRT3 can be a potential therapeutic target. Here we focus on summarizing the intricate mechanisms of SIRT3 in human diseases, and recent notable advances in the field of small-molecule activators or inhibitors targeting SIRT3 as well as their potential therapeutic applications for future drug discovery.

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“…This process is affected by the regulatory effects of Snail, Slug, ZEB1, and Twist1 in the tumor microenvironment. Among all the factors that promote tumor cell migration, ROS play key roles by activating signals that cause cell migration, such as activating the proto-oncogene tyrosine protein kinase (Src) and focal adhesion kinase (FAK)[ 211 ]. The EMT is the initial step of ROS-activated tumor cell migration.…”

Section: Impact Of Ros From Pdt On Cscsmentioning

confidence: 99%

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Zhang

Wang

et al. 2020

WJSC

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Photodynamic therapy (PDT) is an effective and promising cancer treatment. PDT directly generates reactive oxygen species (ROS) through photochemical reactions. This oxygen-dependent exogenous ROS has anti-cancer stem cell (CSC) effect. In addition, PDT may also increase ROS production by altering metabolism, endoplasmic reticulum stress, or potential of mitochondrial membrane. It is known that the half-life of ROS in PDT is short, with high reactivity and limited diffusion distance. Therefore, the main targeting position of PDT is often the subcellular localization of photosensitizers, which is helpful for us to explain how PDT affects CSC characteristics, including differentiation, self-renewal, apoptosis, autophagy, and immunogenicity. Broadly speaking, excess ROS will damage the redox system and cause oxidative damage to molecules such as DNA, change mitochondrial permeability, activate unfolded protein response, autophagy, and CSC resting state. Therefore, understanding the molecular mechanism by which ROS affect CSCs is beneficial to improve the efficiency of PDT and prevent tumor recurrence and metastasis. In this article, we review the effects of two types of photochemical reactions on PDT, the metabolic processes, and the biological effects of ROS in different subcellular locations on CSCs.

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Inhibition of epithelial cell migration and Src/FAK signaling by SIRT3

Cited by 57 publications

References 38 publications

Mitohormesis Primes Tumor Invasion and Metastasis

Mitohormesis Primes Tumor Invasion and Metastasis

Mitochondrial Sirtuin 3: New emerging biological function and therapeutic target

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

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