11-13 May 2012 Helsingør - Denmark www.networkbio.org

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abStractS For PoSterS
ThOMAS R COx1 , ERWIN SChOOf2, SARA zANIVAN3, RUNE LINDING2 AND JANINE T ERLER1
1 BIOTECh RESEARCh AND INNOVATION CENTRE, UNIVERSITY Of COPENhAGEN, DENMARK 2 CENTER
fOR BIOLOGICAL SEqUENCE ANALYSIS, TEChNICAL UNIVERSITY Of DENMARK, DENMARK 3 BEATSON
INSTITUTE fOR CANCER RESEARCh, GLASGOW, UK
Remodelling of the ECM as a critical mediator of tumour metastasis
Tumour metastasis is a highly complex, dynamic and inefficient process involving multiple steps, yet accounts
for over 90% of cancer patient deaths. The tumour microenvironment and in particular the extracellular
matrix is a key component in driving this process at multiple stages. Both the biochemical and biomechanical
properties or tumour extracellular matrix (ECM) contribute to progression. Metastatic tumours show
elevated ECM remodelling and increased stiffness in comparison to their non-metastatic counterparts and
these changes in stiffness are known to drive metastatic cell behaviour although the underlying molecular
mechanisms remain elusive. The aim of this project is to utilise multiple molecular approaches and evaluate
both the molecular and behavioural changes occurring in tumour cells in response to ECM remodelling and
in particular changes in ECM stiffness. By computationally integrating molecular and phenotypic data, we
aim to derive a molecular network associated with stiffness and identify key enablers of metastatic progression.
Using breast and colorectal cancer models, we have found that metastatic tumours are stiffer than matched
non-metastatic tumours. We have shown that increasing ECM stiffness can drive the invasive behaviour of
the non-metastatic cancer cells. We observe associated cell signalling events and gene expression changes,
and are further investigating the molecular networks associated with enhanced metastasis in response
to increased stiffness.
The goal of the study is to predict and test novel therapeutic strategies for the treatment and prevention of
metastasis that could then be translated into the clinic.
30 / INB 2012 • 11-13 May 2012 www.networkbio.org / 31