H2O2 transit through the mitochondrial intermembrane space promotes tumor cell growth in vitro and in vivo

Sabharwal, SimranS.; Dudley, V.Joseph; Landwerlin, Charlène; Schumacker, Paul T.

doi:10.1016/j.jbc.2023.104624

Cited by 9 publications

(2 citation statements)

References 52 publications

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“…Keratin 17 is a vital component of keratin, and is capable of inducing OS cell development and glycolysis, which are indispensable for cellular energy supply by activating the AKT/mTOR/HIF-1α pathway in the underlying mechanism of OS growth ( Yan et al, 2020 ). During the process of OS cell proliferation, mitochondrial H 2 O 2 signal transduction promotes tumor cell proliferation through HIF-1α-dependent and HIF-1α-independent manners ( Sabharwal et al, 2023 ). Another study revealed that HIF-1α and VEGF regulate OS cell apoptosis under hypoxia, and any disruption to one substance may subsequently affect the existence of the other, demonstrating the critical function that HIF-1α and VEGF play in OS apoptosis ( Yang SY.…”

Section: Molecular Mechanisms Of Hif-1α In Osmentioning

confidence: 99%

Hypoxia inducible factor-1ɑ as a potential therapeutic target for osteosarcoma metastasis

Zhou,

Lan,

Liu

et al. 2024

Front. Pharmacol.

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Osteosarcoma (OS) is a malignant tumor originating from mesenchymal tissue. Pulmonary metastasis is usually present upon initial diagnosis, and metastasis is the primary factor affecting the poor prognosis of patients with OS. Current research shows that the ability to regulate the cellular microenvironment is essential for preventing the distant metastasis of OS, and anoxic microenvironments are important features of solid tumors. During hypoxia, hypoxia-inducible factor-1α (HIF-1α) expression levels and stability increase. Increased HIF-1α promotes tumor vascular remodeling, epithelial-mesenchymal transformation (EMT), and OS cells invasiveness; this leads to distant metastasis of OS cells. HIF-1α plays an essential role in the mechanisms of OS metastasis. In order to develop precise prognostic indicators and potential therapeutic targets for OS treatment, this review examines the molecular mechanisms of HIF-1α in the distant metastasis of OS cells; the signal transduction pathways mediated by HIF-1α are also discussed.

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Section: Molecular Mechanisms Of Hif-1α In Osmentioning

confidence: 99%

Hypoxia inducible factor-1ɑ as a potential therapeutic target for osteosarcoma metastasis

Zhou,

Lan,

Liu

et al. 2024

Front. Pharmacol.

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“…PRDX 5 prefers lipid peroxides and peroxynitrite over H 2 O 2 . Artificial PRDX5 expression in IMSp attenuated hypoxic transcriptome reprograming as well as carcinogenesis [ 65 , 66 ]. PRDX6 can be recruited to mitochondria (to OMM) [ 67 , 68 , 69 ].…”

Section: Redox Sources Vs Redox Buffers In Mitochondria and Cytosolmentioning

confidence: 99%

Pitfalls of Mitochondrial Redox Signaling Research

Ježek

2023

Antioxidants

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Redox signaling from mitochondria (mt) to the cytosol and plasma membrane (PM) has been scarcely reported, such as in the case of hypoxic cell adaptation or (2-oxo-) 2-keto-isocaproate (KIC) β-like-oxidation stimulating insulin secretion in pancreatic β-cells. Mutual redox state influence between mitochondrial major compartments, the matrix and the intracristal space, and the cytosol is therefore derived theoretically in this article to predict possible conditions, when mt-to-cytosol and mt-to-PM signals may occur, as well as conditions in which the cytosolic redox signaling is not overwhelmed by the mitochondrial antioxidant capacity. Possible peroxiredoxin 3 participation in mt-to-cytosol redox signaling is discussed, as well as another specific case, whereby mitochondrial superoxide release is diminished, whereas the matrix MnSOD is activated. As a result, the enhanced conversion to H2O2 allows H2O2 diffusion into the cytosol, where it could be a predominant component of the H2O2 release. In both of these ways, mt-to-cytosol and mt-to-PM signals may be realized. Finally, the use of redox-sensitive probes is discussed, which disturb redox equilibria, and hence add a surplus redox-buffering to the compartment, where they are localized. Specifically, when attempts to quantify net H2O2 fluxes are to be made, this should be taken into account.

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Proline and dihydroorotate dehydrogenase promote a hyper-proliferative state and dampen ferroptosis in cancer cells by rewiring mitochondrial redox metabolism

Mailloux

2024

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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H2O2 transit through the mitochondrial intermembrane space promotes tumor cell growth in vitro and in vivo

Cited by 9 publications

References 52 publications

Hypoxia inducible factor-1ɑ as a potential therapeutic target for osteosarcoma metastasis

Hypoxia inducible factor-1ɑ as a potential therapeutic target for osteosarcoma metastasis

Pitfalls of Mitochondrial Redox Signaling Research

Proline and dihydroorotate dehydrogenase promote a hyper-proliferative state and dampen ferroptosis in cancer cells by rewiring mitochondrial redox metabolism

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