Mitochondrial Involvement in Migration, Invasion and Metastasis

Denisenko, Tatiana V.; Горбунова, А. С.; Zhivotovsky, Boris

doi:10.3389/fcell.2019.00355

Cited by 97 publications

(86 citation statements)

References 186 publications

(256 reference statements)

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“…Therefore, FICZ might participate to repair the B[a]P‐induced DNA damage. Bcl2 participates in apoptosis induced by mitochondrial leakage of cytochrome c and plays an important role in the regulation of ROS production and cell migration (Denisenko, Gorbunova, & Zhivotovsky, 2019; Perianayagam, Madias, Pereira, & Jaber, 2010). The regulations of P53 to cell cycle, DNA repair, and apoptosis dependent on ROS generation and caspase activation in mitochondria (Schuler & Green, 2001; Sionov, Hayon, & Haupt, 2013).…”

Section: Discussionmentioning

confidence: 99%

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

Gan

Ding

Chen

2020

Cell Biology International

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Benzo[a]pyrene (B[a]P), a potent carcinogen, has been proved that it can induce apoptosis via activation of the aryl hydrocarbon receptor (AhR) pathway. The metabolite of tryptophan 6‐formylindolo[3,2‐b]carbazole (FICZ), an endogenous activator of AhR, plays bifunctional roles in cell growth and apoptosis. However, whether and how FICZ can reduce the toxicity of B[a]P and the mechanism underlying this remain unclear. In this study, FICZ interfered with the toxicity of B[a]P in mouse hepatocarcinoma cell line Hepa1‐6. The results of the MTT assay indicated that FICZ and B[a]P made opposite effects on cell proliferation. The scratch‐wound healing assay showed that B[a]P (1 µM for 24 hr) exposure triggered cell migration and that was inhibited by FICZ (10 nM). In addition, FICZ ameliorated B[a]P‐induced apoptosis by inhibiting reactive oxygen species generation and caspase‐3 activation, as well as increasing reduced glutathione level in mitochondria. Furthermore, gene expression analyses indicated that FICZ competed with B[a]P, which reduced the transcriptional activation of the cyp1a1 and cyp1b1 genes, as well as Bcl2 and P53. Accordingly, the interaction between FICZ and B[a]P in the AhR pathway inhibited apoptosis in a mitochondrial‐dependent manner, suggesting that endogenous compound may reduce the toxicity of exogenous pollutant in vivo and providing an available way to improve health condition related to the hepatic metabolic disorder.

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Section: Discussionmentioning

confidence: 99%

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

Gan

Ding

Chen

2020

Cell Biology International

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“…Mitochondrial impairments have been associated to several pathologies not only limited to metabolic diseases or myopathies, but including cancer (Vyas et al, 2016;Denisenko et al, 2019), pulmonary hypertension (Chen et al, 2019) and neurodegenerative disorders such as Alzheimer's and Parkinson's disease (Kim and Mook-Jung, 2019;Tapias, 2019). Thus, further understanding of mitochondrial surveillance mechanisms might help to establish therapeutic interventions for treatment of mitochondrial pathologies.…”

Section: Future Perspectivesmentioning

confidence: 99%

Mitochondrial Quality Control Governed by Ubiquitin

Ravanelli

Brave

Hoppe

2020

Front. Cell Dev. Biol.

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Mitochondria are essential organelles important for energy production, proliferation, and cell death. Biogenesis, homeostasis, and degradation of this organelle are tightly controlled to match cellular needs and counteract chronic stress conditions. Despite providing their own DNA, the vast majority of mitochondrial proteins are encoded in the nucleus, synthesized by cytosolic ribosomes, and subsequently imported into different mitochondrial compartments. The integrity of the mitochondrial proteome is permanently challenged by defects in folding, transport, and turnover of mitochondrial proteins. Therefore, damaged proteins are constantly sequestered from the outer mitochondrial membrane and targeted for proteasomal degradation in the cytosol via mitochondrial-associated degradation (MAD). Recent studies identified specialized quality control mechanisms important to decrease mislocalized proteins, which affect the mitochondrial import machinery. Interestingly, central factors of these ubiquitindependent pathways are shared with the ER-associated degradation (ERAD) machinery, indicating close collaboration between both tubular organelles. Here, we summarize recently described cellular stress response mechanisms, which are triggered by defects in mitochondrial protein import and quality control. Moreover, we discuss how ubiquitindependent degradation is integrated with cytosolic stress responses, particularly focused on the crosstalk between MAD and ERAD.

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“…It has been shown that cellular metabolism is involved in cell migration and eventually in metastasis, and that addiction of cancer cells on mitochondria depends on the cancer type (summarized by [43,58,59]). Being at the crossroad of glycolysis, lipid and oxidative metabolism [19,60], mGPDH controls important metabolic functions and may be involved in metabolic adaptations during tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

Role of Mitochondrial Glycerol-3-Phosphate Dehydrogenase in Metabolic Adaptations of Prostate Cancer

Pecinová

Alán

Brázdová

et al. 2020

Cells

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Prostate cancer is one of the most prominent cancers diagnosed in males. Contrasting with other cancer types, glucose utilization is not increased in prostate carcinoma cells as they employ different metabolic adaptations involving mitochondria as a source of energy and intermediates required for rapid cell growth. In this regard, prostate cancer cells were associated with higher activity of mitochondrial glycerol-3-phosphate dehydrogenase (mGPDH), the key rate limiting component of the glycerophosphate shuttle, which connects mitochondrial and cytosolic processes and plays significant role in cellular bioenergetics. Our research focused on the role of mGPDH biogenesis and regulation in prostate cancer compared to healthy cells. We show that the 42 amino acid presequence is cleaved from N-terminus during mGPDH biogenesis. Only the processed form is part of the mGPDH dimer that is the prominent functional enzyme entity. We demonstrate that mGPDH overexpression enhances the wound healing ability in prostate cancer cells. As mGPDH is at the crossroad of glycolysis, lipogenesis and oxidative metabolism, regulation of its activity by intramitochondrial processing might represent rapid means of cellular metabolic adaptations.

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Mitochondrial Involvement in Migration, Invasion and Metastasis

Cited by 97 publications

References 186 publications

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

Mitochondrial Quality Control Governed by Ubiquitin

Role of Mitochondrial Glycerol-3-Phosphate Dehydrogenase in Metabolic Adaptations of Prostate Cancer

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