RB1-mediated cell-autonomous and host-dependent oncosuppressor mechanisms in radiation-induced osteosarcoma

被引：5

作者：

Kansara, Maya ^{[1
]}

Thomas, David M. ^{[1
,2
,3
]}

机构：

[1] Peter MacCallum Canc Ctr, Div Res, Sarcoma Genom & Genet Lab, Melbourne, Vic, Australia

[2] Kinghorn Canc Ctr, Sydney, NSW, Australia

[3] Garvan Inst, Sydney, NSW, Australia

来源：

ONCOIMMUNOLOGY | 2014年 / 3卷 / 01期

关键词：

interleukin-6; natural killer T cells; radiation; retinoblastoma; 1; senescence; senescence-associated secretory phenotype (SASP); INDUCED SENESCENCE; CANCER; MICE;

D O I：

10.4161/onci.27569

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The mechanisms by which retinoblastoma 1 (RB1) mediates oncosuppressive functions are still being elucidated. We found that radiation-induced senescence in the bone depends on RB1 and is associated with the secretion of multiple bioactive factors, including interleukin-6 (IL-6), as well as with the infiltration of natural killer T (NKT) cells. Importantly, the inhibition of RB1, IL-6 or NKT cells predisposed mice to radiation-induced osteosarcomas, unveiling a cancer cell-extrinsic mechanisms that underlie the oncosuppressive activity of RB1.

引用

页数：3

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