Therapy-induced polyploidization and senescence: Coincidence or interconnection?

Sikora, Ewa; Czarnecka‐Herok, Joanna; Bojko, Agnieszka; Sunderland, Piotr

doi:10.1016/j.semcancer.2020.11.015

Cited by 45 publications

(36 citation statements)

References 153 publications

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“…As a matter of fact, the two key characteristics of senescent cells are cell cycle arrest and degradation of proliferation ability (104). This makes the discussion of PGCC always be accompanied by its relationship with the senescence phenotype, just as a couple of recent reviews systematically introduced the complex connections and differences between polyploidy and senescence (105)(106)(107). A handful of common features between polyploidy and senescence were summarized, including induction of DNA damage, activation of P53/Rb, escaping from cell death, growing incidence of autophagy, common associated genes, and recovery of stemness gene (107).…”

Section: Pgccs Behave Numerous Senescent Phenotypesmentioning

confidence: 99%

“…If the two do have a lot in common, this is confusing when many views hold the point that polyploid cells are involved in tumor recurrence (9,13). Sikora and colleagues discussed therapy-induced senescence (TIS) and therapy-induced polyploidy (TIP), unifying their roles in tumor DNA damage response mechanisms and clarifying that senescence and polyploidy are two necessary conditions for neosis to play a role in the repopulation of PGCCs, especially the later one (105). In other words, senescent cells that have failed to undergo polyploidization may not be able to escape the fate of senescence and death in the end, neither returning to the mitotic cycle (105).…”

Section: Pgccs Behave Numerous Senescent Phenotypesmentioning

confidence: 99%

“…Sikora and colleagues discussed therapy-induced senescence (TIS) and therapy-induced polyploidy (TIP), unifying their roles in tumor DNA damage response mechanisms and clarifying that senescence and polyploidy are two necessary conditions for neosis to play a role in the repopulation of PGCCs, especially the later one (105). In other words, senescent cells that have failed to undergo polyploidization may not be able to escape the fate of senescence and death in the end, neither returning to the mitotic cycle (105). This view can explain the recent research on the restoration of proliferative activity of senescent cells induced by antitumor stress (110).…”

Section: Pgccs Behave Numerous Senescent Phenotypesmentioning

confidence: 99%

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Stress-Induced Polyploid Giant Cancer Cells: Unique Way of Formation and Non-Negligible Characteristics

et al. 2021

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Polyploidy is a conserved mechanism in cell development and stress responses. Multiple stresses of treatment, including radiation and chemotherapy drugs, can induce the polyploidization of tumor cells. Through endoreplication or cell fusion, diploid tumor cells convert into giant tumor cells with single large nuclei or multiple small nucleuses. Some of the stress-induced colossal cells, which were previously thought to be senescent and have no ability to proliferate, can escape the fate of death by a special way. They can remain alive at least before producing progeny cells through asymmetric cell division, a depolyploidization way named neosis. Those large and danger cells are recognized as polyploid giant cancer cells (PGCCs). Such cells are under suspicion of being highly related to tumor recurrence and metastasis after treatment and can bring new targets for cancer therapy. However, differences in formation mechanisms between PGCCs and well-accepted polyploid cancer cells are largely unknown. In this review, the methods used in different studies to induce polyploid cells are summarized, and several mechanisms of polyploidization are demonstrated. Besides, we discuss some characteristics related to the poor prognosis caused by PGCCs in order to provide readers with a more comprehensive understanding of these huge cells.

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Section: Pgccs Behave Numerous Senescent Phenotypesmentioning

confidence: 99%

Section: Pgccs Behave Numerous Senescent Phenotypesmentioning

confidence: 99%

Section: Pgccs Behave Numerous Senescent Phenotypesmentioning

confidence: 99%

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Stress-Induced Polyploid Giant Cancer Cells: Unique Way of Formation and Non-Negligible Characteristics

et al. 2021

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“…Ample clinical and experimental findings made with various models support the hypothesis that polyploids formed in a cancer cell population are responsible for its resistance to treatments and can survive chemotherapy and radiotherapy [113,115,140]. Lethality is often attributed to giant polyploid cancer cells, which have higher biological and epigen- etic plasticity and are capable of metastasis [115,145]. Other dangerous properties of these cells are their capabilities of dormancy in response to therapy and rediploidization when normal conditions are restored in their microenvironment.…”

Section: Whole-genome Duplications In Tumor Cellsmentioning

confidence: 99%

Whole-Genome Duplications in Evolution, Ontogeny, and Pathology: Complexity and Emergency Reserves

Anatskaya

Vinogradov

2021

Mol Biol

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Whole-genome duplication (WGD), or polyploidy, increases the amount of genetic information in the cell. WGDs of whole organisms are found in all branches of eukaryotes and act as a driving force of speciation, complication, and adaptations. Somatic-cell WGDs are observed in all types of tissues and can result from normal or altered ontogenetic programs, regeneration, pathological conditions, aging, malignancy, and metastasis. Despite the versatility of WGDs, their functional significance, general properties, and causes of their higher adaptive potential are unclear. Comparisons of whole-transcriptome data and information from various fields of molecular biology, genomics, and molecular medicine showed several common features for polyploidy of organisms and somatic and cancer cells, making it possible to understand what WGD properties lead to the emergence of an adaptive phenotype. The adaptation potential of WGDs may be associated with an increase in the complexity of the regulation of networks and signaling systems; a higher resistance to stress; and activation of ancient evolutionary programs of unicellularity and pathways of morphogenesis, survival, and life extension. A balance between the cell and organismal levels in controlling gene regulation may shift in stress towards the priority of cell survival, and the shift can lead to cardiovascular diseases and carcinogenesis. The presented information helps to understand how polyploidy creates new phenotypes and why it acts as a driving force of evolution and an important regulator of biological processes in somatic cells during ontogeny, pathogenesis, regeneration, and transformation.

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“…Although multinucleated polyploid cells are found in Alzheimer's disease (Sosunov et al 2020) and after various viral infections (Leroy et al 2020), the most prominent presence of polyploid cells exists in cancer. Polyploid giant cancer cells (PGCCs) can arise in virtually all types of cancer and their role in tumor aggressiveness and relapse after therapy have been gaining attention recently (Zhang et al 2021;Pienta et al 2020;Sikora et al 2020;Tagal and Roth 2021;Herbein and Nehme 2020). It should be noted that the effects of polyploidization on tumorigenesis are highly dependent on tissue and cell-type context.…”

Section: Non-cell Autonomous Functions Of Polyploid Cells In Diseasementioning

confidence: 99%

Regulation and function of developmentally controlled polyploidization

Rijnberk¹

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Chapter 1 systems , such as yeast (Harashima et al. 2013). This box provides a general overview of canonical mitotic cell-cycle regulation. Cell cycle regulationProgression through the cell cycle is primarily regulated through the activity of cyclin-dependent kinases (Cdks), a class of enzymes that initiate the processes of each cell cycle phase (Figure 2a). The activity of Cdks during the cell cycle is regulated by their interaction with cyclins. Cyclins are subject to rapid ubiquitination and degradation at defi ned moments during the cell cycle to regulate their cyclical abundance. The anaphase promoting complex/cyclosome (APC/C) and Skp, Cullin, F-box containing complex (SCF complex) are the two main complexes that regulate the degradation of cyclins and other cell-cycle proteins during the cell cycle (Harashima et al. 2013). An additional layer of cell cycle regulation consists of proteins that aff ect the activity of CDK/cyclin complexes, such as cyclin-dependent kinase inhibitor proteins (CKIs) and CDK or cyclin kinases and phosphatases.

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Therapy-induced polyploidization and senescence: Coincidence or interconnection?

Cited by 45 publications

References 153 publications

Stress-Induced Polyploid Giant Cancer Cells: Unique Way of Formation and Non-Negligible Characteristics

Stress-Induced Polyploid Giant Cancer Cells: Unique Way of Formation and Non-Negligible Characteristics

Whole-Genome Duplications in Evolution, Ontogeny, and Pathology: Complexity and Emergency Reserves

Regulation and function of developmentally controlled polyploidization

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