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Targeting aurora kinases limits tumour growth through DNA damage-mediated senescence and blockade of NF-?B impairs this drug-induced senescence
Journal article   Open access   Peer reviewed

Targeting aurora kinases limits tumour growth through DNA damage-mediated senescence and blockade of NF-?B impairs this drug-induced senescence

Yan Liu, Oriana E. Hawkins, Yingjun Su, Anna E. Vilgelm, Tammy Sobolik, Yee-Mon Thu, Sara Kantrow, Ryan C. Splittgerber, Sarah Short, Katayoun I. Amiri, …
EMBO molecular medicine, Vol.5(1), pp.149-166
01/01/2013
DOI: 10.1002/emmm.201201378
PMCID: PMC3569660
PMID: 23180582
url
https://doi.org/10.1002/emmm.201201378View
Published (Version of record) Open Access

Abstract

Oncogene-induced senescence can provide a protective mechanism against tumour progression. However, production of cytokines and growth factors by senescent cells may contribute to tumour development. Thus, it is unclear whether induction of senescence represents a viable therapeutic approach. Here, using a mouse model with orthotopic implantation of metastatic melanoma tumours taken from 19 patients, we observed that targeting aurora kinases with MLN8054/MLN8237 impaired mitosis, induced senescence and markedly blocked proliferation in patient tumour implants. Importantly, when a subset of tumour-bearing mice were monitored for tumour progression after pausing MLN8054 treatment, 50% of the tumours did not progress over a 12-month period. Mechanistic analyses revealed that inhibition of aurora kinases induced polyploidy and the ATM/Chk2 DNA damage response, which mediated senescence and a NF-?B-related, senescence-associated secretory phenotype (SASP). Blockade of IKK beta/NF-?B led to reversal of MLN8237-induced senescence and SASP. Results demonstrate that removal of senescent tumour cells by infiltrating myeloid cells is crucial for inhibition of tumour re-growth. Altogether, these data demonstrate that induction of senescence, coupled with immune surveillance, can limit melanoma growth.
Life Sciences & Biomedicine Medicine, Research & Experimental Research & Experimental Medicine Science & Technology

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