Adenine nucleotide translocase family: four isoforms for apoptosis modulation in cancer

Brenner, Catherine; Subramaniam, K.; Pertuiset, Claire; Pervaiz, Shazib

doi:10.1038/onc.2010.501

Cited by 68 publications

(57 citation statements)

References 111 publications

(137 reference statements)

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“…42,43 ANT normally mediates the exchange of ADP and ATP between the cytosol and the mitochondrial matrix. 44 This enzymatic activity gets impaired on oxidization, resulting in intramitochondrial ADP shortage and inhibited F 1 F O -ATP synthase. 45 Furthermore, several proteomic changes are rapidly triggered in mitochondria by oxidative stress, including the upregulation of (part of) the antioxidant systems listed above as well as of several molecular chaperons that counteract ROS-induced protein unfolding.…”

Section: Mitochondrial Control Of Stress Responsesmentioning

confidence: 99%

Mitochondrial Control of Cellular Life, Stress, and Death

Galluzzi

Kepp²,

Trojel-Hansen³

et al. 2012

Circulation Research

452

318

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Since the discovery that mitochondrial membrane permeabilization represents a critical step in the regulation of intrinsic apoptosis, mitochondria have been viewed as pluripotent organelles, controlling cell death as well as several aspects of cell survival. Mitochondria constitute the most prominent source of ATP and are implicated in multiple anabolic and catabolic circuitries. In addition, mitochondria coordinate cell-wide stress responses, such as autophagy, and control nonapoptotic cell death routines, such as regulated necrosis. Thus, mitochondria seem to regulate a continuum of cellular functions, spanning from physiological metabolism to stress responses and death. The involvement of mitochondria in both vital and lethal processes is crucial for both embryonic and postembryonic development, as well as for the maintenance of adult tissue homeostasis. In line with this notion, primary mitochondrial defects or alterations in the signaling pathways that converge on or emanate from mitochondria underpin a large number of human diseases, including premature aging, neurodegenerative disorders, cardiovascular disorders, and cancer. Here, we provide an overview of the molecular mechanisms that enable mitochondria to sustain cell survival, coordinate stress responses, and mediate cell death, linking these pathways—whenever relevant—to cardiovascular health and disease.

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Section: Mitochondrial Control Of Stress Responsesmentioning

confidence: 99%

Mitochondrial Control of Cellular Life, Stress, and Death

Galluzzi

Kepp²,

Trojel-Hansen³

et al. 2012

Circulation Research

452

318

View full text Add to dashboard Cite

show abstract

“…In addition, ANT2 plays an antiapoptotic role by maintaining the mitochondrial membrane potential (16,17). The above-mentioned unique expression pattern and the biologic function of ANT2 suggested a protumoral role of ANT2; therefore, ANT2 was considered as a promising therapeutic target for cancer treatment.…”

Section: Ant2 Expression In Tumor Tissuesmentioning

confidence: 99%

“…Adenine nucleotide translocase (ANT) is a protein abundant in the inner mitochondrial membrane involving in mitochondrial oxidative phosphorylation and glycolytic metabolism (16)(17)(18). ANT also interacts with BCL2 family proteins and regulates mitochondrial membrane permeability and mitochondria-mediated apoptosis (16)(17)(18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

“…ANT also interacts with BCL2 family proteins and regulates mitochondrial membrane permeability and mitochondria-mediated apoptosis (16)(17)(18)(19)(20). Four isoforms of ANT, encoded by ANT1, ANT2, ANT3, and ANT4 genes, have been identified in humans.…”

Section: Introductionmentioning

confidence: 99%

“…ANT1 is abundantly expressed in terminally differentiated cells. In contrast, ANT2 is highly expressed in undifferentiated cells and tissues with proliferating and regenerating abilities including lymphocytes and the kidneys and liver (16,17,21). ANT2 expression is also higher than ANT1 expression in several types of human cancer cells (17,18,22,23).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Targeting Adenine Nucleotide Translocase-2 (ANT2) to Overcome Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in Non–Small Cell Lung Cancer

Jang

Kim

Nam

et al. 2016

Molecular Cancer Therapeutics

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EGFR tyrosine kinase inhibitor (EGFR-TKI) therapy has achieved favorable clinical outcomes in non-small cell lung cancer (NSCLC) patients with EGFR mutations. However, patients eventually develop resistance to EGFR-TKIs by several mechanisms. Adenine nucleotide translocase-2 (ANT2) is an oncogenic mitochondrial membrane-associated protein. We investigated the therapeutic potential of ANT2 inhibition to EGFR-TKI resistance in NSCLC using gefitinib-sensitive (PC9 and HCC827) and gefitinib-resistant (H1975 and HCC827/ GR) NSCLC cell lines. ANT2 was inhibited by transfecting cells with an ANT2-specific shRNA. ANT2 expression was elevated in the H1975 and HCC827/GR cells compared with the PC9 and HCC827 cells. ANT2 upregulation in gefitinib-resistant cells was associated with increased SP1 binding to the ANT2 promoter. ANT2-specific shRNA decreased NSCLC cell viability.Moreover, ANT2-specific shRNA sensitized the H1975 and HCC827/GR cells to gefitinib, accompanied by HSP90 and EGFR downregulation. ANT2-specific shRNA also inactivated the PI3K/Akt signaling pathway in the H1975 and HCC827/GR cells, which was mediated by the suppression of miR-221/222 levels and by the subsequent restoration of PTEN. In EGFR-TKI-treated NSCLC patients, ANT2 expression was higher in patients exhibiting poor responses compared with patients showing excellent responses. Furthermore, ANT2 expression increased in tumor tissues biopsied after acquiring gefitinib resistance compared with tissues before gefitinib treatment. These findings suggest that ANT2 overexpression contributes to EGFR-TKI resistance in NSCLC and that ANT2 targeting may be considered a novel strategy for overcoming this resistance.

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The transferred translocases: An old wine in a new bottle

Balaji

2021

Biotech and App Biochem

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The role of translocases was underappreciated and was not included as a separate class in the enzyme commission until August 2018. The recent research interests in proteomics of orphan enzymes, ionomics, and metallomics along with high‐throughput sequencing technologies generated overwhelming data and revamped this enzyme into a separate class. This offers a great opportunity to understand the role of new or orphan enzymes in general and specifically translocases. The enzymes belonging to translocases regulate/permeate the transfer of ions or molecules across the membranes. These enzyme entries were previously associated with other enzyme classes, which are now transferred to a new enzyme class 7 (EC 7). The entries that are reclassified are important to extend the enzyme list, and it is the need of the hour. Accordingly, there is an upgradation of entries of this class of enzymes in several databases. This review is a concise compilation of translocases with reference to the number of entries currently available in the databases. This review also focuses on function as well as dysfunction of translocases during normal and disordered states, respectively.

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Adenine nucleotide translocase family: four isoforms for apoptosis modulation in cancer

Cited by 68 publications

References 111 publications

Mitochondrial Control of Cellular Life, Stress, and Death

Mitochondrial Control of Cellular Life, Stress, and Death

Targeting Adenine Nucleotide Translocase-2 (ANT2) to Overcome Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in Non–Small Cell Lung Cancer

The transferred translocases: An old wine in a new bottle

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