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Abstract
Colorectal carcinoma cells Isreco1 display an ability to migrate controlled by a complex set of signals issued from the membrane. By comparing cells infected by mycoplasmas and mycoplasmas free cells, we have established that basal 2D migration is dependent on a double signal mediated by the collagen receptors integrins alpha1/2 and the Toll-Like receptor TLR2. The signal issued from mycoplasmas can be replaced by a TLR2 ligand and the functional effect is neutralized by silencing of MyD88. Following previous observation that downregulation of E-cadherin/p120 catenin increases cell motility, we now report that EGFR or CD44 inhibition have a similar effect on cell motility that is restricted to tetraspanin Co-029/tspan8 transduced IsrecoI cells (Is1-Co029). The modulation of cell migration linked to EGFR or CD44 can be neutralized by antagonizing Co-029 with the mAb Ts29.1 or by RNA interference. Altogether these data point to a crucial role of Co-029 in the modulation of colon cancer cell motility which could be related to the protumoral effect reported for this tetraspanin. Among surface molecules able to mediate Co-029 function, E-cadherin, EGFR and CD44 appear as likely candidates.
Highlights
Cell motility has attracted considerable interest because of its involvement in normal tissue development and repair and in tumor invasion and metastasis [1]
Following previous observation that downregulation of E-cadherin/p120 catenin increases cell motility, we report that EGFR or CD44 inhibition have a similar effect on cell motility that is restricted to tetraspanin Co-029/tspan8 transduced IsrecoI cells (Is1-Co029)
Among multiple colon carcinoma cell lines tested for single cell migration ability on collagen I, only Isreco1 cells transduced or not with the tetraspanin Co029 have a homogeneous pattern of cell migration with a low dispersion of cell speed between individual cells (Supplementary Movie 1 left)
Summary
Cell motility has attracted considerable interest because of its involvement in normal tissue development and repair and in tumor invasion and metastasis [1]. Depending on the cells and their environment, extracellular signals may trigger various aspects of this program. The obvious consequence of these biological activities is that they can be targeted for the treatment of tumors and are widely investigated. We have shown in a previous work that motility of the Isreco colon carcinoma cells is triggered by a collagen I substrate [4]. Whereas Isreco cells don't move on tissue culture plastic (TCP), they become intensely motile in an integrin dependent mechanism when a collagen I substrate is added. These cells display a regular pattern of migration as shown by single cell tracking that demonstrates a low dispersion of cell speed between individual cells.
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