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Exploring the therapeutic potential of mitochondrial uncouplers in cancer

Shrestha, Riya, Johnson, Edward, Byrne, Frances L.·2021·Molecular Metabolism
DOI 10.1016/j.molmet.2021.101222PMC PMC8129951
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Figure 1 Mitochondrial uncouplers increase mitochondrial respiration. Mitochondrial uncouplers mediate proton (H+) transport into the mitochondrial matrix via a pathway independent of ATP synthase [9,10]. Uncouplers bind to protons in the intermembrane space proceeding to cross the inner mitochondrial membrane (IMM). Mitochondrial protonophore uncouplers are typically lipophilic weak acids that can penetrate membranes [18]. Once an uncoupler has crossed the IMM, it is deprotonated and cycles out of the mitochondrial matrix, where it becomes protonated again to continue the uncoupling cycle. This figure was created with BioRender.com and adapted from Demine et al. [17].
Figure 1 Mitochondrial uncouplers increase mitochondrial respiration. Mitochondrial uncouplers mediate proton (H+) transport into the mitochondrial matrix via a pathway independent of ATP synthase [9,10]. Uncouplers bind to protons in the intermembrane space proceeding to cross the inner mitochondrial membrane (IMM). Mitochondrial protonophore uncouplers are typically lipophilic weak acids that can penetrate membranes [18]. Once an uncoupler has crossed the IMM, it is deprotonated and cycles out of the mitochondrial matrix, where it becomes protonated again to continue the uncoupling cycle. This figure was created with BioRender.com and adapted from Demine et al. [17].CC BY-NC-ND · PubMed Central
Figure 2 Relationships between mitochondrial uncoupler-induced phenotypes in cancer cells. Mitochondrial uncouplers induce mitochondrial membrane depolarisation, decrease ATP levels, increase ROS, and decrease anti-oxidant defence by reducing levels of GSH. These phenotypes are linked to changes in signalling pathways including Wnt/β-catenin, AMPK, mTOR, and HIF1α, many of which inhibit cancer cell proliferation and viability (apoptosis). Other phenotypes include arrest in the Go/G1 phase of the cell cycle, altered expression of cell cycle-regulated proteins including cyclin-dependent kinases (CDK), and upregulation of CDK inhibitors such as p21 and p27. Mitochondrial uncouplers also increase opening the mitochondrial permeability transition pore (mPTP), mitochondrial swelling, and rupture of mitochondrial membranes, which leads to calcium and cytochrome c release and subsequent apoptosis (or necrosis) when given in higher doses and longer durations (denoted by ∗). Phenotypes elevated by uncouplers are shown in green boxes, phenotypes decreased by uncouplers are shown in red boxes, and those in the blue boxes show differences in phenotypes (increased or decreased) that are closely related.
Figure 2 Relationships between mitochondrial uncoupler-induced phenotypes in cancer cells. Mitochondrial uncouplers induce mitochondrial membrane depolarisation, decrease ATP levels, increase ROS, and decrease anti-oxidant defence by reducing levels of GSH. These phenotypes are linked to changes in signalling pathways including Wnt/β-catenin, AMPK, mTOR, and HIF1α, many of which inhibit cancer cell proliferation and viability (apoptosis). Other phenotypes include arrest in the Go/G1 phase of the cell cycle, altered expression of cell cycle-regulated proteins including cyclin-dependent kinases (CDK), and upregulation of CDK inhibitors such as p21 and p27. Mitochondrial uncouplers also increase opening the mitochondrial permeability transition pore (mPTP), mitochondrial swelling, and rupture of mitochondrial membranes, which leads to calcium and cytochrome c release and subsequent apoptosis (or necrosis) when given in higher doses and longer durations (denoted by ∗). Phenotypes elevated by uncouplers are shown in green boxes, phenotypes decreased by uncouplers are shown in red boxes, and those in the blue boxes show differences in phenotypes (increased or decreased) that are closely related.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Shrestha, R., Johnson, E., & Byrne, F. L.
ORCID
Venue
Molecular Metabolism
Publisher
Elsevier BV
Published
2021-09
Volume
51
Pages
101222
ISSN
2212-8778
DOI
10.1016/j.molmet.2021.101222
PMC
PMC8129951
Cited by
131
References
13
Language
en
Licence
Funders
  • University of New South Wales
  • Cancer Institute NSW (2018/ECF003)

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