Journal
PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY
Volume 165, Issue -, Pages 3-7Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbiomolbio.2021.05.002
Keywords
Polyploid giant cancer cell (PGCC); Polyaneuploid cancer cell (PACC); Reactive oxygen species; Cell cycle; Therapy resistance
Categories
Funding
- US Department of Defense CDMRP/PCRP [W81XWH-20-10353]
- Patrick C. Walsh Prostate Cancer Research Fund
- Prostate Cancer Foundation
- NCI [U54CA143803, CA163124, CA093900, CA143055]
- William and Carolyn Stutt Research Fund
- Ronald Rose
- MC Dean, Inc.
- William and Marjorie Springer
- Mary and Dave Stevens
- Louis Dorfman
- Jones Family Foundation
- Timothy Hanson
- David and June Trone Family Foundation
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Cancer cells respond to oxidative stress by activating the DNA damage response and entering cell cycle arrest, leading to apoptosis in most cases, but some cells may enter a protected G0 state and become polyaneuploid cancer cells, resulting in resistant tumor growth.
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. (c) 2021 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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