Format

Send to

Choose Destination
Trends Cell Biol. 2016 Mar;26(3):215-226. doi: 10.1016/j.tcb.2015.10.005. Epub 2015 Nov 9.

Non-Cell-Autonomous Regulation of Cellular Senescence in Cancer.

Author information

1
Institute of Oncology Research (IOR), Oncology Institute of Southern Switzerland, Bellinzona 6500, Switzerland.
2
Institute of Oncology Research (IOR), Oncology Institute of Southern Switzerland, Bellinzona 6500, Switzerland; Faculty of Biology and Medicine, University of Lausanne (UNIL), Lausanne 1011, Switzerland. Electronic address: andrea.alimonti@ior.iosi.ch.

Abstract

Cellular senescence is a permanent growth arrest that is broadly recognized to act as a barrier against tumorigenesis. Senescence is predominant in premalignant tumors, and senescence escape is thought to be required for tumor progression. Importantly, evidences indicate that cell-autonomous mechanisms, such as genetic alterations or therapeutic interventions targeting specific genetic pathways, can affect the senescence response in cancer. Nevertheless, new findings have emerged in the last few years that indicate a fundamental role for the tumor microenvironment in the regulation of cellular senescence. Indeed, cytokines belonging to the senescent secretome, as well as tumor-infiltrating immune subsets, have been described to modulate the senescence response in tumors. Such evidence demonstrates that senescence initiation also relies on non-cell-autonomous mechanisms, which are discussed in the present review.

KEYWORDS:

SASP; senescence; tumor immune microenvironment

PMID:
26564316
DOI:
10.1016/j.tcb.2015.10.005
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center