TY - JOUR
T1 - Tumor Promoting Aspects of Senescence in Cancer Progression
AU - Yang, Qing
AU - Xie, Yingqiu
AU - Miao, Lixia
PY - 2016/10/20
Y1 - 2016/10/20
N2 - Cancers induced by gene mutation, deletion, and genome instability might be related to aging. With similar pathways of aging but distinct functions, senescence at the cellular level is an irreversible arrest of cell cycle. Senescence has long been believed as a barrier to restrict tumor expansion. However, more and more evidence has been shown that senescence inducers regulate epithelial–mesenchymal transition, stem cell self-renewal, inflammatory response, crosstalk with the oncogenic bypass signaling, and conversion of oncogene to tumor suppressor. Here we will discuss the most recent findings of the oncogenic aspects of senescence which crosstalk with multiple pathways in cancer progression.
AB - Cancers induced by gene mutation, deletion, and genome instability might be related to aging. With similar pathways of aging but distinct functions, senescence at the cellular level is an irreversible arrest of cell cycle. Senescence has long been believed as a barrier to restrict tumor expansion. However, more and more evidence has been shown that senescence inducers regulate epithelial–mesenchymal transition, stem cell self-renewal, inflammatory response, crosstalk with the oncogenic bypass signaling, and conversion of oncogene to tumor suppressor. Here we will discuss the most recent findings of the oncogenic aspects of senescence which crosstalk with multiple pathways in cancer progression.
KW - cancer
KW - Senescence
UR - http://www.scopus.com/inward/record.url?scp=84992047693&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84992047693&partnerID=8YFLogxK
U2 - 10.1080/07357907.2016.1227443
DO - 10.1080/07357907.2016.1227443
M3 - Review article
AN - SCOPUS:84992047693
SN - 0735-7907
VL - 34
SP - 452
EP - 458
JO - Cancer Investigation
JF - Cancer Investigation
IS - 9
ER -