ROS-induced cell cycle arrest as a mechanism of resistance in polyaneuploid cancer cells (PACCs)

Cancer is responsible for the deaths of millions of people worldwide each year. Once metastasized, the disease is incurable and shows resistance to all anti-cancer therapies. The already-elevated level of reactive oxygen species (ROS) in cancer cells is further increased by therapies. The oxidative...

Full description

Saved in:
Bibliographic Details
Published inProgress in biophysics and molecular biology Vol. 165; pp. 3 - 7
Main Authors Kuczler, Morgan D., Olseen, Athen M., Pienta, Kenneth J., Amend, Sarah R.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.10.2021
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Cancer is responsible for the deaths of millions of people worldwide each year. Once metastasized, the disease is incurable and shows resistance to all anti-cancer therapies. The already-elevated level of reactive oxygen species (ROS) in cancer cells is further increased by therapies. The oxidative stress activates the DNA damage response (DDR) and the stressed cancer cell moves towards cell cycle arrest. Once arrested, the majority of cancer cells will undergo programmed cell death in the form of apoptosis. If the cancer cell is able to exit the cell cycle prior to cell division and enter a protected G0 state, it is able to withstand and survive therapy as a polyaneuploid cancer cell (PACC) and eventually seed resistant tumor growth.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Morgan D. Kuczler: Conceptualization, Writing – Original Draft, Writing – Review & Editing Athen M. Olseen: Conceptualization, Writing – Original Draft, Writing – Review & Editing Kenneth J. Pienta: Writing – Review & Editing, Funding acquisition Sarah R. Amend: Conceptualization, Writing – Review & Editing, Funding acquisition
Author Statement
ISSN:0079-6107
1873-1732
1873-1732
DOI:10.1016/j.pbiomolbio.2021.05.002