Genomic heterogeneity meets cellular energetics: crosstalk between the mitochondria and the cell cycle

Herrera, Erica L.; Azzam, Seham Z.; Berger, Madison C.; Díaz-Martínez, Laura A.

doi:10.20517/2394-4722.2018.35

Cited by 4 publications

(3 citation statements)

References 114 publications

(130 reference statements)

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“…Bi-directional communication between mitochondria and nucleus has been shown to provide the equilibrium of cellular homeostasis. The anterograde signaling consists in the nuclear control of the mitochondria by regulation of nuclear-encoded mitochondrial genes, while the complementary retrograde signaling is aimed to permit mitochondrial communication with the nucleus [54,55].…”

Section: Mito-nuclear Crosstalkmentioning

confidence: 99%

Mitochondrial Involvement in Cisplatin Resistance

Cocetta

Ragazzi

Montopoli

2019

IJMS

102

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Cisplatin is one of the worldwide anticancer drugs and, despite its toxicity and frequent recurrence of resistance phenomena, it still remains the only therapeutic option for several tumors. Circumventing cisplatin resistance remains, therefore, a major goal for clinical therapy and represents a challenge for scientific research. Recent studies have brought to light the fundamental role of mitochondria in onset, progression, and metastasis of cancer, as well as its importance in the resistance to chemotherapy. The aim of this review is to give an overview of the current knowledge about the implication of mitochondria in cisplatin resistance and on the recent development in this research field. Recent studies have highlighted the role of mitochondrial DNA alterations in onset of resistance phenomena, being related both to redox balance alterations and to signal crosstalk with the nucleus, allowing a rewiring of cell metabolism. Moreover, an important role of the mitochondrial dynamics in the adaptation mechanism of cancer cells to challenging environment has been revealed. Giving bioenergetic plasticity to tumor cells, mitochondria allow cells to evade death pathways in stressful conditions, including chemotherapy. So far, even if the central role of mitochondria is recognized, little is known about the specific mechanisms implicated in the resistance. Nevertheless, mitochondria appear to be promising pharmacological targets for overcoming cisplatin resistance, but further studies are necessary.

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Section: Mito-nuclear Crosstalkmentioning

confidence: 99%

Mitochondrial Involvement in Cisplatin Resistance

Cocetta

Ragazzi

Montopoli

2019

IJMS

102

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“…The crosstalk between the nucleus and mitochondria is crucial since in the yeast S. cerevisiae, all but sixteen (thirteen in Homo sapiens ) mitochondrial proteins are encoded by the nuclear genome [ 58 , 110 ]. Many nuclear genes are involved in the replication, transcription, integrity, and segregation of mitochondrial DNA.…”

Section: Resultsmentioning

confidence: 99%

Yeast Chromatin Mutants Reveal Altered mtDNA Copy Number and Impaired Mitochondrial Membrane Potential

Staneva

Vasileva

Podlesniy

et al. 2023

JoF

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Mitochondria are multifunctional, dynamic organelles important for stress response, cell longevity, ageing and death. Although the mitochondrion has its genome, nuclear-encoded proteins are essential in regulating mitochondria biogenesis, morphology, dynamics and function. Moreover, chromatin structure and epigenetic mechanisms govern the accessibility to DNA and control gene transcription, indirectly influencing nucleo-mitochondrial communications. Thus, they exert crucial functions in maintaining proper chromatin structure, cell morphology, gene expression, stress resistance and ageing. Here, we present our studies on the mtDNA copy number in Saccharomyces cerevisiae chromatin mutants and investigate the mitochondrial membrane potential throughout their lifespan. The mutants are arp4 (with a point mutation in the ARP4 gene, coding for actin-related protein 4—Arp4p), hho1Δ (lacking the HHO1 gene, coding for the linker histone H1), and the double mutant arp4 hho1Δ cells with the two mutations. Our findings showed that the three chromatin mutants acquired strain-specific changes in the mtDNA copy number. Furthermore, we detected the disrupted mitochondrial membrane potential in their chronological lifespan. In addition, the expression of nuclear genes responsible for regulating mitochondria biogenesis and turnover was changed. The most pronounced were the alterations found in the double mutant arp4 hho1Δ strain, which appeared as the only petite colony-forming mutant, unable to grow on respiratory substrates and with partial depletion of the mitochondrial genome. The results suggest that in the studied chromatin mutants, hho1Δ, arp4 and arp4 hho1Δ, the nucleus-mitochondria communication was disrupted, leading to impaired mitochondrial function and premature ageing phenotype in these mutants, especially in the double mutant.

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“…These genetic alterations predominantly arise from chromosomal instability, itself driven by tetraploidy (e.g., from centrosome aberrations) [ 32 ], as from other mutagenic processes. Moreover, mitochondrial dysfunctions may also induce nuclear genome instability and conversely ( Figure 2 ) [ 33 ].…”

Section: Types and Mechanisms Of Heterogeneitymentioning

confidence: 99%

Dynamic Cancer Cell Heterogeneity: Diagnostic and Therapeutic Implications

Jacquemin

Antoine

Dom

et al. 2022

Cancers

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Though heterogeneity of cancers is recognized and has been much discussed in recent years, the concept often remains overlooked in different routine examinations. Indeed, in clinical or biological articles, reviews, and textbooks, cancers and cancer cells are generally presented as evolving distinct entities rather than as an independent heterogeneous cooperative cell population with its self-oriented biology. There are, therefore, conceptual gaps which can mislead the interpretations/diagnostic and therapeutic approaches. In this short review, we wish to summarize and discuss various aspects of this dynamic evolving heterogeneity and its biological, pathological, clinical, diagnostic, and therapeutic implications, using thyroid carcinoma as an illustrative example.

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Genomic heterogeneity meets cellular energetics: crosstalk between the mitochondria and the cell cycle

Cited by 4 publications

References 114 publications

Mitochondrial Involvement in Cisplatin Resistance

Mitochondrial Involvement in Cisplatin Resistance

Yeast Chromatin Mutants Reveal Altered mtDNA Copy Number and Impaired Mitochondrial Membrane Potential

Dynamic Cancer Cell Heterogeneity: Diagnostic and Therapeutic Implications

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