Cellular Senescence As a Target in Cancer Control

Overview

Journal J Aging Res

Publisher Wiley

Specialty Geriatrics

Date 2011 Jan 15

PMID 21234095

Citations 18

Authors

Mar Vergel

Juan J Marin

Purificacion Estevez

Amancio Carnero

Affiliations

Soon will be listed here.

Abstract

Somatic cells show a spontaneous decline in growth rate in continuous culture. This is not related to elapsed time but to an increasing number of population doublings, eventually terminating in a quiescent but viable state termed replicative senescence. These cells are commonly multinucleated and do not respond to mitogens or apoptotic stimuli. Cells displaying characteristics of senescent cells can also be observed in response to other stimuli, such as oncogenic stress, DNA damage, or cytotoxic drugs and have been reported to be found in vivo. Most tumors show unlimited replicative potential, leading to the hypothesis that cellular senescence is a natural antitumor program. Recent findings suggest that cellular senescence is a natural mechanism to prevent undesired oncogenic stress in somatic cells that has been lost in malignant tumors. Given that the ultimate goal of cancer research is to find the definitive cure for as many tumor types as possible, exploration of cellular senescence to drive towards antitumor therapies may decisively influence the outcome of new drugs. In the present paper, we will review the potential of cellular senescence to be used as target for anticancer therapy.

Citing Articles

Petroleum ether extract of induces senescence and inhibits invasion in breast cancer MDA-MB-231 cells.

Long T, Phuong L, Van Nguyen Dang L, Ngoc T, Thao D, Trinh N 3 Biotech. 2025; 15(2):45.

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Therapy-induced senescence in breast cancer: an overview.

Chembukavu S, Lindsay A Explor Target Antitumor Ther. 2024; 5(4):902-920.

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Senescent Cells: Dual Implications on the Retinal Vascular System.

Habibi-Kavashkohie M, Scorza T, Oubaha M Cells. 2023; 12(19).

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Fitting parameters and therapies of ODE tumor models with senescence and immune system.

Guillen-Gonzalez F, Sevillano-Castellano E, Suarez A J Math Biol. 2023; 87(5):67.

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Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer.

Kallenbach J, Atri Roozbahani G, Heidari Horestani M, Baniahmad A Cell Biosci. 2022; 12(1):200.

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