Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Proffered Paper - Basic Science

1O - A study of cancer dissemination from metastatic intermediates of hypermethylated colorectal patients reveals a new mode of collective migration


21 Sep 2020


Proffered Paper - Basic Science


Emmanuel Dornier


Annals of Oncology (2020) 31 (suppl_4): S245-S259. 10.1016/annonc/annonc265


E. Dornier1, D. Pagès1, M.P. Ducreux2, D. Malka3, F. Jaulin1

Author affiliations

  • 1 Inserm U1279, Institut Gustave Roussy, 94805 - Villejuif/FR
  • 2 Medical Oncology, Gustave Roussy Cancer Center, 94805 - Villejuif/FR
  • 3 Digestive Oncology, Institut Gustave Roussy, 94805 - Villejuif/FR


Login to access the resources on OncologyPRO.

Abstract 1O


Colorectal cancer (CRC) is the second most deadly cancer. Amongst the different types of CRCs, the hypermethylated subtype (CIMP) is the most aggressive. In a previous study, we identified that CIMP CRCs are able to form a new metastatic intermediate consisting of clusters of a hundred cells found in the peritoneal cavity of metastatic patients. Furthermore, these collective structures can also be found in the primary tumour. Importantly, when invading they only exist as collectives and do not show any sign of adhesion with the extracellular matrix or cell protrusion which are characteristics of collective mesenchymal migration, the only mode of collective dissemination described to date. These data suggest that CIMP clusters are using a new mode of invasion resembling the amoeboid movement of single cells, never described before.


We used microfluidics coated with non-adhesive polymer.


We find that CIMP and colorectal cell line clusters confined in non-adhesive microchannels are able to move, independently of the formation of focal adhesions or protruding leader cells. Their migration speed ranged between 70 to 150μm/day, in line with observed cancer spread in vivo. We show that clusters display a supra-cellular actin cortex with increased contractility towards the rear of moving clusters, indicated by Myosin-II accumulation. This is a typical feature of amoeboid motion, where Rho activity is more intense towards the back. Indeed, interfering with ROCK or myosin activation strongly opposed migration. Moreover, using optogenetic tools we show that Rho activation at the back of the cluster is sufficient to promote migration.


By studying primary cancer specimens and cell lines from colorectal cancer, we demonstrate the existence of a second mode of collective migration, presenting the hallmarks of amoeboid migration, that we named collective amoeboid. This mode could be use by other cancer clusters when confronted to non-adhesive interfaces like the lumen of lymphatic vessels. This work suggests that therapies targeting adhesive properties of cancer cells might be unsuccessful and unravels a new therapeutic avenue to limit the metastatic spread of CRCs.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.


Has not received any funding.


All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings