A recurrent chromosomal inversion suffices for driving escape from oncogene-induced senescence via subTAD reorganization

Zampetidis, Christos P.; Galanos, Panagiotis; Angelopoulou, Andriani; Zhu, Yeping; Polyzou, Aikaterini; Karamitros, Timokratis; Kotsinas, Athanassios; Lаgopati, Nefeli; Mourkioti, Ioanna; Mirzazadeh, Reza; Polyzos, A.; Garnerone, Silvano; Mizi, Athanasia; Gusmao, Eduardo Gade; Sofiadis, Konstantinos; Gál, Zita; Larsen, Dorthe Helena; Pefani, Dafni-Eleftheria; Demaria, Marco; Tsirigos, Aristotelis; Crosetto, Nicola; Maya-Mendoza, Apolinar; Papaspyropoulos, Angelos; Evangelou, Konstantinos; Bártek, Jiří; Papantonis, Argyris; Gorgoulis, Vassilis G.

doi:10.1016/j.molcel.2021.10.017

Cited by 32 publications

(41 citation statements)

References 102 publications

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“…Notably, CDC6 mediated genomic instability, triggered genetic alterations, which were followed by chromatin reshaping and remodeling during EOIS. 4 Among the accumulated genetic rearrangements, we observed a recurrent inversion on chromosome 3. This event, in combination with the consequent reshuffling of the regional chromatin, resulted in reactivation of a dormant replication origin and upregulation of Basic Helix-Loop-Helix Family Member E40 ( BHLHE40 ), a transcription factor that is involved in the regulation of circadian clock machinery.…”

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confidence: 92%

“…For this purpose, we exploited our recently generated Cell Division Cycle 6 (CDC6)-overexpressing normal cellular epithelial system, as the CDC6 replication licensing factor possesses potent oncogenic properties 4 (and references therein). Notably, CDC6 mediated genomic instability, triggered genetic alterations, which were followed by chromatin reshaping and remodeling during EOIS.…”

mentioning

confidence: 99%

“…This event, in combination with the consequent reshuffling of the regional chromatin, resulted in reactivation of a dormant replication origin and upregulation of Basic Helix-Loop-Helix Family Member E40 ( BHLHE40 ), a transcription factor that is involved in the regulation of circadian clock machinery. 4 Given that increasing amount of data connectthe circadian clock with the coordination of the cell cycle, deregulations of circadian rhythm effectors might in turn disrupt the physiological cell cycle process conferring a detrimental impact at the organism level. 5 The latter is reflected in various pathological processes, setting the grounds for further investigation.…”

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confidence: 99%

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Escape from senescence: revisiting cancer therapeutic strategies

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“…The protocol provided is tailored to HBECs; however, it can be readily applied to additional adherent cellular models. For complete details on the use and execution of this protocol, please refer to Zampetidis et al. (2021) .…”

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confidence: 99%

“…For complete details on the use and execution of this protocol, please refer to Zampetidis et al. (2021) .…”

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CRISPR-Cas9-mediated induction of large chromosomal inversions in human bronchial epithelial cells

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Targeting senescence as an anticancer therapy

Bousset

Gil

2022

Molecular Oncology

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Cellular senescence is a stress response elicited by different molecular insults. Senescence results in cell cycle exit and is characterised by multiple phenotypic changes such as the production of a bioactive secretome. Senescent cells accumulate during ageing and are present in cancerous and fibrotic lesions. Drugs that selectively kill senescent cells (senolytics) have shown great promise for the treatment of age-related diseases. Senescence plays paradoxical roles in cancer. Induction of senescence limits cancer progression and contributes to therapy success, but lingering senescent cells fuel progression, recurrence, and metastasis.In this review, we describe the intricate relation between senescence and cancer. Moreover, we enumerate how current anti-cancer therapies induce senescence in tumour cells and how senolytic agents could be deployed to complement anticancer therapies. "One-two punch" therapies aim to first induce senescence in the tumour followed by senolytic treatment to target newly exposed vulnerabilities in senescent tumour cells. "One-two punch" represents an emerging and promising new strategy in cancer treatment. Future challenges of "one -two punch" approaches include how to best monitor senescence in cancer patients to effectively survey their efficacy.

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A recurrent chromosomal inversion suffices for driving escape from oncogene-induced senescence via subTAD reorganization

Cited by 32 publications

References 102 publications

Escape from senescence: revisiting cancer therapeutic strategies

Escape from senescence: revisiting cancer therapeutic strategies

CRISPR-Cas9-mediated induction of large chromosomal inversions in human bronchial epithelial cells

Targeting senescence as an anticancer therapy

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