The antagonistic relationship between apoptosis and polyploidy in development and cancer
One of the important functions of regulated cell death is to prevent cells from inappropriately acquiring extra copies of their genome, a state known as polyploidy. Apoptosis is the primary cell death mechanism that prevents polyploidy, and defects in this apoptotic response can result in polyploid...
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Published in | Seminars in cell & developmental biology Vol. 156; pp. 35 - 43 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Ltd
15.03.2024
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Abstract | One of the important functions of regulated cell death is to prevent cells from inappropriately acquiring extra copies of their genome, a state known as polyploidy. Apoptosis is the primary cell death mechanism that prevents polyploidy, and defects in this apoptotic response can result in polyploid cells whose subsequent error-prone chromosome segregation are a major contributor to genome instability and cancer progression. Conversely, some cells actively repress apoptosis to become polyploid as part of normal development or regeneration. Thus, although apoptosis prevents polyploidy, the polyploid state can actively repress apoptosis. In this review, we discuss progress in understanding the antagonistic relationship between apoptosis and polyploidy in development and cancer. Despite recent advances, a key conclusion is that much remains unknown about the mechanisms that link apoptosis to polyploid cell cycles. We suggest that drawing parallels between the regulation of apoptosis in development and cancer could help to fill this knowledge gap and lead to more effective therapies. |
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AbstractList | One of the important functions of regulated cell death is to prevent cells from inappropriately acquiring extra copies of their genome, a state known as polyploidy. Apoptosis is the primary cell death mechanism that prevents polyploidy, and defects in this apoptotic response can result in polyploid cells whose subsequent error-prone chromosome segregation are a major contributor to genome instability and cancer progression. Conversely, some cells actively repress apoptosis to become polyploid as part of normal development or regeneration. Thus, although apoptosis prevents polyploidy, the polyploid state can actively repress apoptosis. In this review, we discuss progress in understanding the antagonistic relationship between apoptosis and polyploidy in development and cancer. Despite recent advances, a key conclusion is that much remains unknown about the mechanisms that link apoptosis to polyploid cell cycles. We suggest that drawing parallels between the regulation of apoptosis in development and cancer could help to fill this knowledge gap and lead to more effective therapies. One of the important functions of regulated cell death is to prevent cells from inappropriately acquiring extra copies of their genome, a state known as polyploidy. Apoptosis is the primary cell death mechanism that prevents polyploidy, and defects in this apoptotic response can result in polyploid cells whose subsequent error-prone chromosome segregation are a major contributor to genome instability and cancer progression. Conversely, some cells actively repress apoptosis to become polyploid as part of normal development or regeneration. Thus, although apoptosis prevents polyploidy, the polyploid state can actively repress apoptosis. In this review, we discuss progress in understanding the antagonistic relationship between apoptosis and polyploidy in development and cancer. Despite recent advances, a key conclusion is that much remains unknown about the mechanisms that link apoptosis to polyploid cell cycles. We suggest that drawing parallels between the regulation of apoptosis in development and cancer could help to fill this knowledge gap and lead to more effective therapies.One of the important functions of regulated cell death is to prevent cells from inappropriately acquiring extra copies of their genome, a state known as polyploidy. Apoptosis is the primary cell death mechanism that prevents polyploidy, and defects in this apoptotic response can result in polyploid cells whose subsequent error-prone chromosome segregation are a major contributor to genome instability and cancer progression. Conversely, some cells actively repress apoptosis to become polyploid as part of normal development or regeneration. Thus, although apoptosis prevents polyploidy, the polyploid state can actively repress apoptosis. In this review, we discuss progress in understanding the antagonistic relationship between apoptosis and polyploidy in development and cancer. Despite recent advances, a key conclusion is that much remains unknown about the mechanisms that link apoptosis to polyploid cell cycles. We suggest that drawing parallels between the regulation of apoptosis in development and cancer could help to fill this knowledge gap and lead to more effective therapies. |
Author | Herriage, Hunter C. Huang, Yi-Ting Calvi, Brian R. |
AuthorAffiliation | 1: Department of Biology, Indiana University, Bloomington, IN 47405 |
AuthorAffiliation_xml | – name: 1: Department of Biology, Indiana University, Bloomington, IN 47405 |
Author_xml | – sequence: 1 givenname: Hunter C. surname: Herriage fullname: Herriage, Hunter C. – sequence: 2 givenname: Yi-Ting surname: Huang fullname: Huang, Yi-Ting – sequence: 3 givenname: Brian R. surname: Calvi fullname: Calvi, Brian R. email: bcalvi@indiana.edu |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37331841$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_jep_2024_118811 crossref_primary_10_1093_genetics_iyad208 crossref_primary_10_3389_fcell_2024_1410637 crossref_primary_10_1016_j_ijbiomac_2024_131706 crossref_primary_10_3390_genes15010096 crossref_primary_10_3390_ijms25084185 crossref_primary_10_3892_or_2024_8760 crossref_primary_10_1016_j_canlet_2025_217447 crossref_primary_10_1093_genetics_iyae009 |
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Keywords | PGCC Polyploidy devEC WGD iEC Tetraploid Regulated cell death Endoreplication Aneuploidy CNV CDK Apoptosis |
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SubjectTerms | Aneuploidy Apoptosis Apoptosis - genetics Chromosome Segregation Endoreplication Genomic Instability Humans Neoplasms - genetics Polyploidy Regulated cell death Tetraploid |
Title | The antagonistic relationship between apoptosis and polyploidy in development and cancer |
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