CSB: An Emerging Actionable Target for Cancer Therapy

Proietti-De-Santis, Luca; Balzerano, Alessio; Prantera, Giorgio

doi:10.1016/j.trecan.2018.01.005

Cited by 13 publications

(8 citation statements)

References 15 publications

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“…Hence, in the absence of functional CSB, cells are unable to react to hypoxic stimuli and to activate transcription of crucial pro-survival genes. Therefore, suppression of CSB activity might reduce the hypoxia tolerance of tumor cells, thus increasing their apoptotic threshold ( Proietti-De-Santis et al, 2018 ).…”

Section: The Unbalance Of Cs Proteins In Aging and Cancermentioning

confidence: 99%

A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer

2022

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DNA repair genes are critical for preserving genomic stability and it is well established that mutations in DNA repair genes give rise to progeroid diseases due to perturbations in different DNA metabolic activities. Cockayne Syndrome (CS) is an autosomal recessive inheritance caused by inactivating mutations in CSA and CSB genes. This review will primarily focus on the two Cockayne Syndrome proteins, CSA and CSB, primarily known to be involved in Transcription Coupled Repair (TCR). Curiously, dysregulated expression of CS proteins has been shown to exhibit differential health outcomes: lack of CS proteins due to gene mutations invariably leads to complex premature aging phenotypes, while excess of CS proteins is associated with carcinogenesis. Thus it appears that CS genes act as a double-edged sword whose loss or gain of expression leads to premature aging and cancer. Future mechanistic studies on cell and animal models of CS can lead to potential biological targets for interventions in both aging and cancer development processes. Some of these exciting possibilities will be discussed in this review in light of the current literature.

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Section: The Unbalance Of Cs Proteins In Aging and Cancermentioning

confidence: 99%

A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer

2022

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“…Likewise, 50% of AML patients with somatic TP53 mutations exhibited chromosomal rearrangements, whereas the percentage of wild-type TP53 samples with chromothripsis patterns is just 1% . Noteworthy, the loss of p53 functionality can be determined not only by inactivating mutations of the same gene, but also by hyperactivation of proteins involved in its negative modulation [Proietti-De-Santis et al, 2003, 2018Caputo et al, 2013Caputo et al, , 2017.…”

Section: Mechanisms Of (Epi)genetic Variability In Cancermentioning

confidence: 99%

Evolutionary Mechanisms of Cancer Suggest Rational Therapeutic Approaches

Balzerano

Paccosi

Proietti-De-Santis

2021

Cytogenet Genome Res

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The goal in personalized therapeutic approaches for cancer medicine is to identify specific mutations with prognostic and therapeutic value in order to tailor the therapy for the single patient. The most powerful obstacle for personalized medicine arises from intratumor heterogeneity and clonal evolution, which can promote drug resistance. In this scenario, new technologies, such as next-generation sequencing, have emerged as a central diagnostic tool to profile cancer (epi)genomic landscapes. Therefore, a better understanding of the biological mechanisms underlying cancer evolution is mandatory and represents the current challenge to accurately predict whether cancer will recur after chemotherapy with the aim to tailor rational therapeutic approaches.

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“…WRN and BLM are segmental progerias, with the onset of advanced aging symptoms presenting in the second decade of life, while CS and HG patients exhibit a failure-to-thrive phenotype from birth. CSB can promote cell proliferation via the degradation of p53, and knockdown of CSB sensitizes cancer cells to chemotherapeutic-induced apoptosis (Proietti-De-Santis et al 2018). Additionally, CS cells are resistant to UV-induced mutagenesis, which may explain the lack of cancer in CS (Reid-Bayliss et al 2016).…”

Section: Figurementioning

confidence: 99%

NAD⁺ Metabolism in Aging and Cancer

Demarest

Babbar

Okur

et al. 2019

Annu. Rev. Cancer Biol.

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Aging is a major risk factor for many types of cancer, and the molecular mechanisms implicated in aging, progeria syndromes, and cancer pathogenesis display considerable similarities. Maintaining redox homeostasis, efficient signal transduction, and mitochondrial metabolism is essential for genome integrity and for preventing progression to cellular senescence or tumorigenesis. NAD+ is a central signaling molecule involved in these and other cellular processes implicated in age-related diseases and cancer. Growing evidence implicates NAD+ decline as a major feature of accelerated aging progeria syndromes and normal aging. Administration of NAD+ precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) offer promising therapeutic strategies to improve health, progeria comorbidities, and cancer therapies. This review summarizes insights from the study of aging and progeria syndromes and discusses the implications and therapeutic potential of the underlying molecular mechanisms involved in aging and how they may contribute to tumorigenesis.

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CSB: An Emerging Actionable Target for Cancer Therapy

Cited by 13 publications

References 15 publications

A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer

A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer

Evolutionary Mechanisms of Cancer Suggest Rational Therapeutic Approaches

NAD⁺ Metabolism in Aging and Cancer

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CSB: An Emerging Actionable Target for Cancer Therapy

Cited by 13 publications

References 15 publications

A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer

A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer

Evolutionary Mechanisms of Cancer Suggest Rational Therapeutic Approaches

NAD+ Metabolism in Aging and Cancer

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Resources

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NAD⁺ Metabolism in Aging and Cancer