mGluR1 regulates TNBC migration and invasion.

<p>MCF10AT1 or MCF10CA1d cells were transduced either with pLenti-<i>GRM1</i>, pLenti-<i>LacZ</i>, sh<i>GRM1</i>, or NS control. 2.5×10⁵ cells were plated on polycarbonate containing cell inserts and migration or invasion towards chemoattractant (10% serum) was measured after 24 hours. For invasion assays, polycarbonate membranes were coated with reconstituted basement membrane. <b>A. mGluR1 stimulates MCF10AT1 migration.</b> <i>GRM1</i> overexpression in MCF10AT1 cells significantly increased migration of the cells compared to the control <i>LacZ</i> cells, which was reversed (<b>B</b>) by silencing with sh<i>GRM1</i>. <b>C. MCF10AT1 invasion.</b> GRM1 overexpression significantly stimulated the invasion of MCF10AT1 cells through polycarbonate membranes coated with reconstituted basement membrane. <b>D. MCF10CA1d invasion.</b> <i>shGRM1</i> knockdown inhibited the invasion of malignant MCF10CA1d cells compared to the NS transduced cells. Results are recorded as the mean ± SEM of three experiments, where *p<0.05 compared to control. <b>Legend</b>: NS = nonsilencing control; sh<i>GRM1</i> = shRNA against <i>GRM1</i>; <i>LacZ</i> = pLenti-<i>LacZ</i>; <i>GRM1</i> = pLenti-<i>GRM1</i>.