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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Genome-wide CRISPR/Cas9 library screen identifies PCMT1 as a critical driver of ovarian cancer metastasis

Fig. 2

PCMT1 contributes to metastasis-associated tumor cell phenotypes. A PCMT1 knockout in SKOV3 cells was verified via western blotting (left) and DNA sequencing (right). B Cell proliferation of the control and PCMT1-knockout SKOV3 cells was assessed every 24 h for 5 days using the CCK-8 assay. C The living cell counts of control SKOV3 and PCMT1 knockout SKOV3 cells after a 5-day spheroid formation assay. D Wound healing assays of control SKOV3 and PCMT1 knockout SKOV3 cells were performed at 0, 24, and 48 h after the cells were scratched. Up, representative images, down, quantification of migration distance. E Representative images of the cell adhesion assay (left) and analyses of adhesion capacity (right) comparing control SKOV3 and PCMT1 knockout SKOV3 cells (using laminin). F Representative images and quantification of the cell invasion assay comparing control SKOV3 and PCMT1 knockout SKOV3 cells. G Over 5 days of spheroid formation in control OVCAR3 cells and PCMT1-silenced OVCAR3 cells, the numbers of viable cells were counted after trypsin digestion and trypan blue staining. H After ULA cultured for 72 h, the amounts of apoptotic-antiapoptotic proteins were examined in PCMT1 silenced OVCAR3 and SKOV3 cells. Quantification of cell migration distance (I), cell adhesion capacity (using laminin) (J), and cell invasion (K) in the control, PCMT1-knockout and PCMT1-reexpressing SKOV3 cells. (scale bar: 200 μm; Data are shown as mean ± SEM of 3 independent experiments. Data were statistically analyzed with Student's t-test. *P < 0.05; **P < 0.01; ***P < 0.001.)

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