Mitophagy: Link to cancer development and therapy

Куликов, А. В.; Luchkina, Ekaterina A.; Gogvadze, Vladimir; Zhivotovsky, Boris

doi:10.1016/j.bbrc.2016.10.088

Cited by 101 publications

(101 citation statements)

References 92 publications

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“…Mitophagy has been reported to play dual roles in cancer cells: 34 it facilitates cell survival by allowing adaptations to stress or promotes cell death through the excessive removal of mitochondria. 35 Sentelle et al showed that mitophagy induction promotes tumor cell death via a mechanism involving autophagy. 36 To investigate the specific role of PINK1/ Parkin-mediated mitophagy in ZnO NP-induced toxicity, we transfected cells with GFP-LC3 to locate the autophagosomes and used the red fluorescent PINK1 puncta to identify the damaged mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Zinc oxide nanoparticles induce toxicity in CAL 27 oral cancer cell lines by activating PINK1/Parkin-mediated mitophagy

Wang¹,

Gao²,

Wang³

et al. 2018

IJN

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BackgroundTongue squamous cell carcinoma (tongue cancer) is one of the most common malignancies in the oral maxillofacial region. The tumor easily relapses after surgery, and the prognosis remains poor. Recently, zinc oxide nanoparticles (ZnO NPs) were shown to target multiple cancer cell types. In this study, we aimed to elucidate the anticancer effect of ZnO NPs on CAL 27 human tongue cancer cells and identify the role of PINK1/Parkin-mediated mitophagy in this effect.Materials and methodsWe analyzed the dose-dependent cytotoxic effects of ZnO NPs on CAL 27 cells. Cells were cultured in media containing 0, 5, 10, 20, 30, 40, 50, 60, 70, 80, 90, or 100 μg/mL ZnO NPs for 24 h. We further examined the intracellular reactive oxygen species levels, monodansylcadaverine intensity and mitochondrial membrane potential following the administration of 25 μg/mL ZnO NPs for 4, 8, 12, or 24 h and investigated the role of PINK1/Parkin-mediated mitophagy in ZnO NP-induced toxicity in CAL 27 cells.ResultsThe viability of CAL 27 cells decreased after treatment with increasing ZnO NP concentrations. The inhibitory concentration 50% of the ZnO NPs was calculated as 25 μg/mL. The ZnO NPs increased the intracellular reactive oxygen species levels and decreased the mitochondrial membrane potential in a time-dependent manner as well as activated the PINK1/Parkin-mediated mitophagy process in CAL 27 cells.ConclusionBased on our findings, ZnO NPs may possess potential anticancer activity toward tongue cancer cells.

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Section: Discussionmentioning

confidence: 99%

Zinc oxide nanoparticles induce toxicity in CAL 27 oral cancer cell lines by activating PINK1/Parkin-mediated mitophagy

Wang¹,

Gao²,

Wang³

et al. 2018

IJN

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“…Mfn-2 is connected to mitophagy via its possible interaction with Parkin activity in which Parkin stimulates the generation of autophagosome that engulfs PINK1/Parkin-independent mitophagy is mediated by microtubule-associated protein 1 light chain 3 (LC3) that brings mitochondria to autophagosome for mitophagy (Zhang, 2015). LC3 family of proteins provide a mechanism for regulation of defective mitochondrial delivery to autophagosomes (Kulikov et al, 2017). The point here is that the role for melatonin in authophagy induction is an early and temporary effect (Ordoñez et al, 2015).…”

Section: Mitochondrial Mitophagy and Autophagy In Hcc And The Rolesmentioning

confidence: 99%

“…Mitophagy is in association with colocalization (Prieto‐Domínguez et al, ), a process through which mitochondria is delivered to lysosomes for degradation (Prieto‐Domínguez et al, ). In fact, evaluation of colocalization is used to confirm a functional association between lysosomes and autophagosomes (Ordoñez et al, ), double‐membrane structures that are intended for degradation and digestion of cellular organelles and proteins (Kulikov et al, ). Mitochondria and lysosome colocalization is stimulated in HCC cells after incubation with the combination of melatonin and sorafenib (Prieto‐Domínguez et al, ) (Figure ).…”

Section: Introductionmentioning

confidence: 99%

Human hepatocellular carcinoma: Protection by melatonin

Mortezaee

2018

Journal Cellular Physiology

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Despite great scientific breakthroughs toward understanding the identity of human hepatocellular carcinoma (HCC) mechanistically, there are still no clinically efficient therapeutic methods for this cancer. Melatonin (N-acetyl-5-methoxytryptamine) is a multi-tasking hormone that has long been known for its anti-cancer activity against various human cancers including HCC, which is a focus of this review. PubMed database was searched for relevant articles with the keywords: hepatocellular carcinoma (HCC), melatonin, apoptosis, proliferation, invasion, angiogenesis, autophagy, oxidative stress, tumor immunity, and mitogen-activated protein kinase (MAPK) focusing on just human cell lines and English language articles. Melatonin inhibits apoptosis resistance and activates both extrinsic and intrinsic pathways of apoptosis in HCC. Melatonin induces ensoplasmic reticulum (ER)- and autophagy-mediated apoptosis in cancer cells. Melatonin works against cancer cell proliferation, motility, and invasiveness by modulating actions of a variety of transcription factors and related pathways. Melatonin also relieves an immunosuppressive state in HCC cancer cells through making a control over tumor-derived exosomes. Both pro-and anti-oxidative functions of melatonin are necessary for combating HCC. Combination of melatonin with chemotherapy could also provide cumulative effects on cancer cells. Melatonin exerts most of these roles by acting on the members of MAPK family.

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“…An important mechanism of cell protection from excess mtROS is based on inducing the selective autophagy of mitochondria (mitophagy). Mithophagy results in the isolation and subsequent degradation of damaged mitochondria that may be the main source of ROS (Fivenson et al, 2017;Kulikov, Luchkina, Gogvadze, & Zhivotovsky, 2017). Impairment of autophagy processes causes accumulation of damaged cell structures (in particular, mitochondria), ROS buildup in the cell, and as a consequence, inflammatory processes and fibrosis in adjacent tissues (Lee, Wu, et al, 2016;Sun et al, 2017).…”

Section: Formation Of Ros Including Superoxide and Hydrogen Peroxide Inmentioning

confidence: 99%

The role of mitochondrial ROS in antibacterial immunity

Пинегин

Vorobjeva

Pashenkov

et al. 2017

Journal Cellular Physiology

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Reactive oxygen species (ROS) are essential participants of various innate immune cell responses against microorganisms and are also involved in many cellular regulatory pathways. It was believed that the main pool of ROS in the innate immune cells is generated by the NADPH oxidase enzymatic complex. However, it was discovered recently that mitochondrial ROS (mtROS) are equally important for the functioning of the immune system. mtROS play an important role in the development of the antimicrobial innate immune responses. The present mini-review summarizes the most recent data on the role of mtROS in the antibacterial immunity. The principles of mtROS formation and possible mechanisms of their generation under the activation of innate immunity are highlighted in this review. We also speculate on the possibilities of using activators of mtROS production in clinical practice.

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Mitophagy: Link to cancer development and therapy

Cited by 101 publications

References 92 publications

Zinc oxide nanoparticles induce toxicity in CAL 27 oral cancer cell lines by activating PINK1/Parkin-mediated mitophagy

Zinc oxide nanoparticles induce toxicity in CAL 27 oral cancer cell lines by activating PINK1/Parkin-mediated mitophagy

Human hepatocellular carcinoma: Protection by melatonin

The role of mitochondrial ROS in antibacterial immunity

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