Bystander Communication and Cell Cycle Decisions After DNA Damage

Overview

Journal Front Genet

Date 2015 Mar 17

PMID 25774166

Citations 7

Authors

Himjyot Jaiswal

Arne Lindqvist

Affiliations

Soon will be listed here.

Abstract

The DNA damage response (DDR) has two main goals, to repair the damaged DNA and to communicate the presence of damaged DNA. This communication allows the adaptation of cellular behavior to minimize the risk associated with DNA damage. In particular, cell cycle progression must be adapted after a DNA-damaging insult, and cells either pause or terminally exit the cell cycle during a DDR. As cells can accumulate mutations after a DDR due to error-prone DNA repair, terminal cell cycle exit may prevent malignant transformation. The tumor suppressor p53 plays a key role in promoting terminal cell cycle exit. Interestingly, p53 has been implicated in communication of a stress response to surrounding cells, known as the bystander response. Recently, surrounding cells have also been shown to affect the damaged cell, suggesting the presence of intercellular feedback loops. How such feedback may affect terminal cell cycle exit remains unclear, but its presence calls for caution in evaluating cellular outcome without controlling the cellular surrounding. In addition, such feedback may contribute to how the cellular environment affects malignant transformation after DNA damage.

Citing Articles

High-LET-Radiation-Induced Persistent DNA Damage Response Signaling and Gastrointestinal Cancer Development.

Kumar K, Kumar S, Datta K, Fornace Jr A, Suman S Curr Oncol. 2023; 30(6):5497-5514.

PMID: 37366899 PMC: 10297158. DOI: 10.3390/curroncol30060416.

Advances in the Current Understanding of How Low-Dose Radiation Affects the Cell Cycle.

Khan M, Wang Y Cells. 2022; 11(3).

PMID: 35159169 PMC: 8834401. DOI: 10.3390/cells11030356.

Coupling of cell fate selection model enhances DNA damage response and may underlie BE phenomenon.

Demirkiran G, Kalayci Demir G, Guzelis C IET Syst Biol. 2020; 14(2):96-106.

PMID: 32196468 PMC: 8687165. DOI: 10.1049/iet-syb.2019.0081.

Induction of DNA Damages upon Marek's Disease Virus Infection: Implication in Viral Replication and Pathogenesis.

Bencherit D, Remy S, Le Vern Y, Vychodil T, Bertzbach L, Kaufer B J Virol. 2017; 91(24).

PMID: 28978699 PMC: 5709610. DOI: 10.1128/JVI.01658-17.

Reevaluation of ATR signaling in primary resting chronic lymphocytic leukemia cells: evidence for pro-survival or pro-apoptotic function.

Beyaert M, Starczewska E, Perez A, Vanlangendonck N, Saussoy P, Tilman G Oncotarget. 2017; 8(34):56906-56920.

PMID: 28915641 PMC: 5593612. DOI: 10.18632/oncotarget.18144.

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