Fig. 2

Knockdown of DDR1 causes an anti-tumor effect on oral cancer cells a: Western blot analysis of Bcl-2, cleaved caspase 3 and PARP in OEC-M1 and TW2.6 cells following DDR1 knockdown (shDDR1-D1 and –A1) for 48 h. GAPDH was used as an internal control. b: Colony formation assay after knockdown of DDR1 in OEC-M1 and TW2.6 cells for 10 days (left). The mean number of colonies for each well was determined from three independent assays (right). c: Growth rates of OEC-M1 and TW2.6 cells measured by MTT assay after DDR1 knockdown. d: Left: Dot plot for flow cytometric analysis of apoptotic cells after DDR1 knockdown (shDDR1-D1 and –A1) in OEC-M1 and TW2.6 cells for 48 h. Annexin V⁻/PI⁻: viable cells (lower left quadrant), Annexin V⁻/PI⁺: necroticcells (upper left quadrant), Annexin V⁺/PI⁻: early apoptotic cells (lower rightquadrant), Annexin V⁺/PI⁺: late apoptotic cells (upper right quadrant). Right: Bar graph quantifying the percentage of, early apoptotic (early), late apoptotic (late) and necrotic cells (necrosis) according to DDR1 knockdown (shDDR1-D1 and –A1). All data are presented as mean ± SD; *p < 0.05; **p < 0.01; ***p < 0.001 versus non-targeting shRNA plasmid (control)